Salusin-beta
The sticky prosalusin peptide that speeds foam-cell formation in the laboratory and runs high in the blood of many people with heart and vessel disease
Salusin-beta was found in 2003 by a computer search of human gene transcripts. It is cut from the same precursor as salusin-alpha, and in cells and animals the two pull in opposite directions: salusin-beta made macrophages and smooth muscle cells store cholesterol and made plaques larger in mice, while salusin-alpha did the reverse. It also acts in the rat brain on blood pressure and thirst. In people it has only been measured, and its blood level is higher in many, though not all, studies of coronary disease, diabetes and hypertension. It is not a medicine and has no human dose.
No established human dose Details ↓
Recommended Dosing
No established human dose
Salusin-beta has never been given to people in any study read. The human evidence is measurement only: assays that confirm the intact peptide in plasma and urine, and observational comparisons of its blood level in coronary disease, diabetes, hypertension, dialysis, lupus, pancreatitis and other conditions.
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What is it?
Salusin-beta is a 20-amino-acid peptide made from the same precursor as its sister, salusin-alpha. The two were found together in 2003 by a computer search of human gene transcripts rather than by purifying them from tissue. Their precursor, prosalusin, is made from an alternatively spliced message of the TOR2A gene, and salusin-beta is cut from the stretch just before salusin-alpha. Unlike its sister, it is not recorded with an amidated end, and it is unusually sticky: it clings so firmly to plastic and glass that it can vanish from a lab tube before anyone measures it.
That stickiness shaped the whole field. Early tests could not find salusin-beta reliably, and it took a radioimmunoassay in 2009, a sandwich ELISA in 2013 and mass spectrometry in 2017 to show that the intact peptide really circulates in human blood and leaves in urine. Its plasma level swings through the day, lowest in the early morning, and the free peptide falls quickly when vagal activity rises, which fits with its effects on the nervous system in rats. The 2017 work also found seven natural fragments, a reminder that antibody tests may count more than the whole peptide.
In the laboratory, salusin-beta looks like a promoter of artery disease. It made human macrophages and smooth muscle cells store cholesterol and turn into foam cells, raised adhesion and inflammatory signals in vessel-lining cells through NF-kappaB, and made aortic plaques larger in mice prone to atherosclerosis. Where the same experiment tested both peptides, salusin-alpha either pushed the other way or lacked the effect, which is why the two are often described as a pair with opposing roles. Other work points well beyond the artery wall: in rats and mice salusin-beta acts in the brain to lower blood pressure, curb thirst and raise reproductive hormones, it protected dopamine neurons in a Parkinson's model, it killed some bacteria in the dish, and one group identified ATP synthase on the cell surface as a binding site, while a second named the receptor MrgprA1 for its effect on neurons.
In people, salusin-beta has only been measured, never given. Many observational studies report it higher in coronary artery disease, coronary slow flow, type 2 diabetes, hypertension that does not dip at night, haemodialysis, lupus and severe pancreatitis, and one analysis found it a better marker of coronary narrowing than salusin-alpha. Not every study agrees: it was unchanged in pre-eclampsia, lower in people with an aortic aneurysm, and in children with obesity it was raised without tracking severity. Reported values also range from picograms per millilitre to nanomoles per litre depending on the kit, so numbers from different papers cannot be compared directly.
Salusin-beta is not a medicine anywhere and has no human dose. Its effects come from cells and animals, and the human evidence is blood tests in mostly small, single-centre studies that show association, not cause. A high level going with heart disease does not show that lowering it would help, and none of the laboratory treatment ideas, from blocking it in vessels to giving it for Parkinson's disease, has been tried in people. Its sister peptide has its own entry, salusin-alpha, which covers the protective half of the pair.
Mechanism of Action
Salusin-beta is cut from prosalusin and acts on macrophages, vessel-wall cells and brain circuits in laboratory work; two binding sites have been proposed, cell-surface ATP synthase and the receptor MrgprA1.
One precursor, two peptides
Prosalusin comes from an alternatively spliced TOR2A message and is cut into salusin-beta and salusin-alpha, which act in opposite directions on foam cells and plaques in the studies read.
Brain and nerve actions
In rats it lowered blood pressure from the vagal brainstem through NAD(P)H oxidase-derived superoxide, cut water intake when given into the brain, and released vasopressin from the pituitary; in mice it protected dopamine neurons through MrgprA1.
Published Research
These are studies of salusin-beta itself, read from their PubMed abstracts: the discovery paper, the assays that confirmed it in human blood and urine, observational studies comparing its blood level between patients and controls, and cell and animal work in which the peptide was given, silenced or blocked. No study read gave salusin-beta to a person.
Found by searching the human genome's transcripts
A computer screen of full-length human gene transcripts turned up two related peptides, 20 and 28 residues long, that the authors named salusin-beta and salusin-alpha. Both come from one precursor made from an alternatively spliced message of the TOR2A gene, which belongs to the torsion dystonia family. When either was injected into a vein in rats, blood pressure and heart rate dropped fast and far. In the same work salusin-beta made the rat pituitary release vasopressin, and both peptides were picked up in human tissues, plasma and urine.
In coronary plaques, and it speeds foam-cell formation
Both salusins were stained in human coronary plaques, with salusin-beta the stronger signal in the smooth muscle cells and fibroblasts of the lesion. In macrophages grown from human blood monocytes, salusin-beta raised the amount of stored cholesterol ester and roughly doubled the cholesterol-storing enzyme ACAT-1, with the largest effect at a sub-nanomolar concentration. Salusin-alpha did the opposite. Blockers of G-protein, c-Src, protein kinase C and MEK signalling removed the effect, and neither peptide changed cholesterol uptake or export.
First assay in human plasma and urine
Salusin-beta turned out to cling to the polypropylene and polystyrene of ordinary lab tubes, so a solution of it could lose most of its peptide before measurement. Working around that, the authors built a radioimmunoassay aimed at the peptide's C-terminal end, with almost no cross-reaction to salusin-alpha. Chromatography of extracted plasma and urine showed one main peak in the same place as synthetic salusin-beta, and urine from 10 healthy people held 0.23 to 2.22 nmol/L. This confirmed that the peptide circulates and is excreted intact, cut where the gene predicted.
Released by human monocytes and macrophages
Two human monocyte-like cell lines, THP-1 and U937, released salusin-beta into their culture fluid, and the measured material ran on chromatography exactly like the synthetic peptide. When the cells were pushed to mature into macrophages they released several times more, apparently because they cut the precursor faster. The inflammatory signals TNF-alpha and bacterial lipopolysaccharide also raised release without switching on the gene, which points to faster secretion of stored peptide.
Four weeks of infusion enlarged plaques in mice
Apolipoprotein E-deficient mice, a strain that develops atherosclerosis, received a steady infusion of salusin-beta, salusin-alpha or saline from implanted pumps. After four weeks the salusin-beta mice had aortic lesions 2.6 times the size of controls. Their peritoneal macrophages formed foam cells 1.9 times as readily and carried more of the scavenger receptors CD36 and SR-A and of ACAT-1. Salusin-alpha lowered cholesterol and shrank lesions instead.
Where it sits in the rat body
Antibody staining of rat tissues placed salusin-beta mainly in the neuroendocrine and blood-forming systems, a different pattern from salusin-alpha, which was spread through nerve fibres and the linings of organs. In extracts of rat urine the main measured peak ran with synthetic rat salusin-beta. That supports cutting of the rat precursor into both peptides even though the usual pair of basic residues that marks a cleavage site is missing between them.
Drives vessel-wall inflammation through NF-kappaB
In cultured human umbilical vein endothelial cells, salusin-beta raised the adhesion molecule VCAM-1, the chemokine MCP-1, IL-1beta and the oxidant enzyme NOX2, and made monocytes stick to the cell layer; salusin-alpha did not reproduce the NF-kappaB activation. Blocking NF-kappaB stopped the effect, and blocking PI3K also reduced it. In LDL receptor-deficient mice, an antiserum against salusin-beta damped the same inflammatory signals in the aortic lining and kept monocytes from attaching.
No difference in pre-eclampsia
In 48 women with pre-eclampsia and 21 with healthy pregnancies, serum salusin-beta and salusin-alpha were much the same in both groups and did not separate the mild and severe forms. Apelin, measured from the same samples, was the only one of the three peptides that was higher in pre-eclampsia.
A sandwich ELISA for total plasma salusin-beta
Using antibodies to both ends of the peptide, and again working around its stickiness, the group set up a sandwich ELISA. Healthy volunteers had 1.9 to 6.6 nmol/L in plasma, and a single peak matched the synthetic peptide. Levels did not move with posture, a salt infusion or smoking, all strong vasopressin triggers, but they swung through the day, highest in daytime and lowest in the early morning. People with diabetes, coronary disease or cerebrovascular disease had clearly higher levels than healthy controls, as did patients with pituitary failure and central diabetes insipidus.
Worse lesions and inflammation in ApoE-deficient mice
Young apolipoprotein E-deficient mice received salusin-beta, salusin-alpha or vehicle by pump for eight weeks. With salusin-beta the aortic lesions were clearly worse and the inflammatory markers IL-6, TNF-alpha, VCAM-1 and MCP-1 were higher, although blood lipids matched the vehicle group. Salusin-beta also sped the breakdown of I-kappaB-alpha and the move of NF-kappaB into the nucleus, which salusin-alpha did not; salusin-alpha instead eased the lesions and raised HDL cholesterol.
Kills some Gram-positive bacteria
Salusin-beta was strongly active against several Gram-positive species in the dish, among them Staphylococcus aureus, Staphylococcus epidermidis and two Bacillus strains, and it made the membrane of S. aureus leak a fluorescent dye. Five related analogues pointed to the N-terminal part of the peptide as the region the antibacterial effect depends on, and in solution the peptide took up a helical shape.
Higher in teenagers with true high blood pressure
Adolescents were sorted by 24-hour ambulatory monitoring into essential hypertension or white-coat hypertension. The median serum salusin-beta was higher in the essential hypertension group. Across the cohort it rose with body mass index Z-score, office and daytime blood pressure, triglycerides and the triglyceride to HDL ratio, so the authors proposed a part for it in early hypertension and asked for further work.
Higher with more coronary disease
Among 278 consecutive people having coronary angiography, the 160 found to have coronary artery disease had higher serum salusin-beta by ELISA than the 118 without it (about 4.65 versus 3.94 nmol/L). In a multivariate model it stayed independently linked to the presence of disease, and it rose modestly with the angiographic atherosclerosis score (r = 0.316). A group of 126 healthy controls was also measured.
Opposite effects on drinking in mice
Injected under the skin of mice, salusin-beta made them drink more water without changing food intake or movement, and atropine, which blocks muscarinic receptors, removed the effect. Tiny amounts injected into the brain's fluid spaces did the reverse: water intake and activity fell through the whole night-time active phase, and an antibody against salusin-beta given into the brain first prevented it. The authors call it a strong natural thirst suppressant in the brain.
Turns vascular smooth muscle cells toward foam cells
In human vascular smooth muscle cells, salusin-beta led to lipid droplets and more stored cholesterol and made monocytes stick, by raising ACAT-1 and VCAM-1. Silencing either target, blocking NF-kappaB, scavenging oxidants, removing the oxidant enzyme NOX2 or knocking down the microRNA miR155 each undid the effect, which mapped a chain from miR155 through NOX2 and NF-kappaB.
Mass spectrometry confirms the native peptide
After heavy enrichment of human plasma, liquid chromatography with tandem mass spectrometry found full-length salusin-beta and seven natural fragments of it. A new ELISA built to read only the free, intact peptide showed a deep low point in the early morning and a quick fall when parasympathetic (vagal) activity was stepped up. The authors note that older antibody tests may have been counting fragments as well.
Part of high-glucose damage to vessel-lining cells
Human umbilical vein endothelial cells grown in high glucose made more salusin-beta, and they grew, migrated and formed vessel-like tubes less well. Silencing salusin-beta with a viral shRNA restored those functions and reduced cell death, shifting Bcl-2, Bax and caspase-3 in the protective direction. It also lifted the high-glucose block on the energy sensor AMPK, and an AMPK inhibitor cancelled the protection.
More in ovarian tumours, with shorter survival
In 57 ovarian cancer specimens, salusin-beta was higher in tumour than in matched nearby normal tissue, and high levels went with a more advanced FIGO stage, lymph-node spread and shorter overall survival. In SKOV3 ovarian cancer cells, added salusin-beta sped growth and the shift toward a mobile, invasive cell type, with signs of Wnt/beta-catenin activation.
Its receptor: ATP synthase on the cell surface
The authors embedded membrane proteins taken straight from animal tissue into artificial liposomes to search for what salusin-beta binds. The answer was the beta chain of ATP synthase sitting on the cell surface; standard detergent methods had found only a beta-actin and profilin complex inside. Salusin-beta blocked that surface enzyme's activity and stopped tumour-driven blood-vessel growth in a mouse air-sac model, so the authors describe it as an inhibitor of new vessel growth.
Protected dopamine neurons in a Parkinson's model
In mice, salusin-beta protected the dopamine neurons of the midbrain that are lost in Parkinson's disease, and given through the nose in a mouse model of the disease it raised how many of those neurons survived. The effect ran through the receptor MrgprA1: blocking that receptor removed the protection. The authors propose salusin-beta as a treatment candidate, which has not been tested in people.
Much higher in coronary slow flow
Thirty-nine people whose coronary arteries filled slowly on angiography, without blockages, were compared with 42 people with normal angiograms. Median serum salusin-beta was 1,205 pg/mL against 162 pg/mL, and it tracked the frame count that measures how slowly contrast moves (r = 0.564). With body mass index it was one of only two independent predictors of slow flow.
Higher on haemodialysis
In 180 people on haemodialysis, mean salusin-beta was about 1,080 pg/mL against about 268 pg/mL in 90 healthy controls, and salusin-alpha was higher too. Among the dialysis patients, a higher salusin-beta to salusin-alpha ratio went with a thicker carotid wall and faster pulse wave velocity, both signs of vessel ageing, although the links were weak.
A better marker of coronary narrowing than salusin-alpha
In 256 people having coronary angiography for chest pain, ELISA levels of the two salusins together accounted for about three quarters of the spread in the SYNTAX stenosis score. Salusin-beta carried the larger, positive weight (standardised coefficient 0.797) and salusin-alpha a smaller, negative one (-0.367), so the authors rate salusin-beta the more useful of the two.
Lowers blood pressure from the vagal brainstem
In anaesthetised rats, salusin-beta was found in the intermediate part of the dorsal motor nucleus of the vagus. Microinjected there, it reduced sympathetic nerve traffic to the kidney and raised vagal activity, lowering blood pressure and heart rate. The vagal effect depended on superoxide made by NAD(P)H oxidase in that nucleus, and the sympathetic effect also needed GABA-A receptors in the hypothalamus. The rats' own salusin-beta there appeared to keep sympathetic activity in check at rest.
Raised reproductive hormones in male rats
A week of salusin-beta infused into the brain ventricles of male rats increased the hypothalamic message for gonadotropin-releasing hormone and raised blood LH, FSH and testosterone compared with untreated and sham-infused rats. The testes, however, showed narrower seminiferous tubules and a thinner germinal layer.
Higher when blood pressure does not dip at night
Among 88 people with newly diagnosed hypertension, the 47 whose pressure did not fall at night had higher serum salusin-beta than the 41 whose pressure dipped normally (about 576 versus 516 pg/mL by an electrochemiluminescence test), and lower salusin-alpha. Salusin-beta remained an independent predictor of the non-dipping pattern alongside left ventricular mass.
Higher in coronary disease of any extent
In 168 people having coronary angiography, salusin-beta and C-reactive protein were lower in the 55 with normal arteries than in the groups with mild narrowing, one diseased vessel or several. Salusin-beta did not separate the disease groups from one another, and salusin-alpha did not differ between any group.
Higher in type 2 diabetes, highest with poor control
Serum salusin-beta by commercial ELISA was higher in 55 people with type 2 diabetes than in 35 healthy volunteers, and higher again in patients with HbA1c above 9%. Within the patient group it rose with fasting glucose and HbA1c, while salusin-alpha moved the other way. Body weight made no difference to either.
Lower, not higher, with an aortic aneurysm
In 48 people with an abdominal aortic aneurysm and 47 matched people without one, plasma salusin-beta was lower in the aneurysm group and fell as the aorta widened. Arterial stiffness readings did not differ. The authors point out that this runs against the higher levels reported in atherosclerosis, even though the two conditions share risk factors.
Higher in lupus, especially with kidney involvement
Serum salusin-beta averaged about 474 pg/mL in 60 people with systemic lupus erythematosus against about 158 pg/mL in 30 matched controls. It did not track overall disease activity or age, but it was higher in patients with lupus nephritis or thrombosis, and those links held after adjustment; it was lower in patients with serositis.
Higher in severe acute pancreatitis
In 64 people admitted with acute pancreatitis and 18 healthy adults, serum salusin-beta changed between the first and third hospital day, and on both days it was higher in severe disease by the Revised Atlanta criteria than in mild or moderate disease. The authors give cut-off values for spotting severe cases (about 179 pg/mL on day 1) and call for larger studies.
Higher in children with obesity, but not linked to severity
In 125 children with obesity and 33 healthy-weight peers, both salusins were higher in the children with obesity. Unlike salusin-alpha, salusin-beta did not climb with more severe obesity and showed no link to body mass index or C-reactive protein, so the authors favoured salusin-alpha as the earlier marker in this group.
No Established Human Dose
Salusin-beta has never been given to people in any study read. The human evidence is measurement only: assays that confirm the intact peptide in plasma and urine, and observational comparisons of its blood level in coronary disease, diabetes, hypertension, dialysis, lupus, pancreatitis and other conditions. The amounts injected, infused or given into the brain of rats and mice are animal research conditions and do not translate into a human amount, so there is no dose to state.
What this rests on: PMID 19660505, PMID 24098553, PMID 28811505.
Educational information, not medical advice. The doses on this page come from approved labels, published studies and, where no study exists, amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes Salusin-beta is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
Unknown: no human dose of Salusin-beta has been established (see No Established Human Dose below), so there is no amount to work out. The reconstitution calculator does the arithmetic for any vial, water and dose.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Salusin-beta, before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long Salusin-beta stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Salusin-beta. What the human studies gave and how is set out under No Established Human Dose.
What to expect, and when
Unknown: no cited half-life and no label or trial duration on this page says how long Salusin-beta lasts or how long it was given. Results reported in the studies are under Published Research.
Side effects, and when to stop or get help
From the Side Effects section: In the discovery study, an intravenous injection in rats caused a fast, steep fall in blood pressure and heart rate (PMID 12910263); A week of infusion into the brain of male rats narrowed the seminiferous tubules of the testes (PMID 34015344); No human safety data exist: every human study read only measured it (PMID 24098553). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Salusin-beta. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Salusin-beta has not been given to people, so no human side effects are known”).
Interactions
Unknown: a PubMed search for human interaction studies of Salusin-beta (reviewed 2026-11-03) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of Salusin-beta products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder; it checks the measured mass against Salusin-beta's expected mass, 2,342.9 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a medicine anywhere in the sources read: Drugs@FDA (openFDA) returns no record for salusin (November 3, 2026)). Sport: Not on the 2026 List.
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
Salusin-beta has not been given to people, so no human side effects are known.
Contraindications & Cautions
No product label exists. These cautions follow from the evidence.
Legal Status
Salusin-beta is an endogenous research peptide; it is not approved as a medicine anywhere in the sources read.
Frequently Asked Questions
?What is salusin-beta?
A 20-amino-acid peptide cut from prosalusin, the precursor that also yields salusin-alpha. It was identified in 2003 by a computer search of human gene transcripts and has since been confirmed in human plasma and urine by antibody tests and mass spectrometry.
?Is salusin-beta a drug or a supplement?
Neither. No medicine contains it, no regulator has approved it, and no study read has given it to a person. In people it has only been measured.
?How is it different from salusin-alpha?
They share a precursor but are different peptides, 20 and 28 residues long. In cell and animal work salusin-beta increased foam-cell formation and plaque size, while salusin-alpha reduced both.
?Does a high salusin-beta level mean heart disease?
Many studies found higher levels in coronary disease, diabetes and some forms of hypertension, but others found no difference or lower levels, the assays disagree, and no clinical test uses it. It is a research marker, not a diagnosis.
?Why is it hard to measure?
The peptide sticks to plastic and glass, so it can be lost from a sample before testing, and blood also holds fragments of it that some antibody tests may count. Each research group had to design around this, which is one reason published values differ so much.
?Is there a safe dose?
No dose exists. The only amounts ever given were to rats and mice in laboratory studies, and those cannot be turned into a human amount.
References
- [pubmed] Shichiri M, et al. "Salusins: newly identified bioactive peptides with hemodynamic and mitogenic activities." Nat Med, 2003;9(9):1166-72. PMID: 12910263.
- [pubmed] Watanabe T, et al. "Impact of salusin-alpha and -beta on human macrophage foam cell formation and coronary atherosclerosis." Circulation, 2008;117(5):638-48. PMID: 18212280.
- [pubmed] Sato K, et al. "Presence of immunoreactive salusin-beta in human plasma and urine." Regul Pept, 2009;158(1-3):63-7. PMID: 19660505.
- [pubmed] Sato K, et al. "Release of salusin-beta from human monocytes/macrophages." Regul Pept, 2010;162(1-3):68-72. PMID: 20176058.
- [pubmed] Nagashima M, et al. "Chronic infusion of salusin-alpha and -beta exerts opposite effects on atherosclerotic lesion development in apolipoprotein E-deficient mice." Atherosclerosis, 2010;212(1):70-7. PMID: 20684826.
- [pubmed] Suzuki N, et al. "Distinct systemic distribution of salusin-α and salusin-β in the rat." Peptides, 2011;32(4):805-10. PMID: 21193001.
- [pubmed] Koya T, et al. "Salusin-β accelerates inflammatory responses in vascular endothelial cells via NF-κB signaling in LDL receptor-deficient mice in vivo and HUVECs in vitro." Am J Physiol Heart Circ Physiol, 2012;303(1):H96-105. PMID: 22561298.
- [pubmed] Simsek Y, et al. "Serum levels of apelin, salusin-alpha and salusin-beta in normal pregnancy and preeclampsia." J Matern Fetal Neonatal Med, 2012;25(9):1705-8. PMID: 22533552.
- [pubmed] Fujimoto K, et al. "Circulating levels of human salusin-β, a potent hemodynamic and atherogenesis regulator." PLoS One, 2013;8(10):e76714. PMID: 24098553.
- [pubmed] Zhou CH, et al. "Salusin-β not salusin-α promotes vascular inflammation in ApoE-deficient mice via the I-κBα/NF-κB pathway." PLoS One, 2014;9(3):e91468. PMID: 24621517.
- [pubmed] Kimura M, et al. "Salusin-β, an antimicrobially active peptide against Gram-positive bacteria." Chem Pharm Bull (Tokyo), 2014;62(6):586-90. PMID: 24881665.
- [pubmed] Kołakowska U, et al. "Is the serum level of salusin-β associated with hypertension and atherosclerosis in the pediatric population?." Pediatr Nephrol, 2015;30(3):523-31. PMID: 25245503.
- [pubmed] Liu J, et al. "Serum salusin-β levels are associated with the presence and severity of coronary artery disease." J Investig Med, 2015;63(4):632-5. PMID: 25730454.
- [pubmed] Suzuki-Kemuriyama N, et al. "Salusin-β as a powerful endogenous antidipsogenic neuropeptide." Sci Rep, 2016;6:20988. PMID: 26869388.
- [pubmed] Sun HJ, et al. "Salusin-β induces foam cell formation and monocyte adhesion in human vascular smooth muscle cells via miR155/NOX2/NFκB pathway." Sci Rep, 2016;6:23596. PMID: 27004848.
- [pubmed] Fujimoto K, et al. "Identification and quantification of plasma free salusin-β, an endogenous parasympathomimetic peptide." Sci Rep, 2017;7(1):8275. PMID: 28811505.
- [pubmed] Zhu X, et al. "Salusin-β mediates high glucose-induced endothelial injury via disruption of AMPK signaling pathway." Biochem Biophys Res Commun, 2017;491(2):515-521. PMID: 28647373.
- [pubmed] Zhang Q, et al. "Overexpression of salusin-β is associated with poor prognosis in ovarian cancer." Oncol Rep, 2017;37(3):1826-1832. PMID: 28184918.
- [pubmed] Shichiri M, et al. "Identification of the salusin-β receptor using proteoliposomes embedded with endogenous membrane proteins." Sci Rep, 2018;8(1):17865. PMID: 30552345.
- [pubmed] Chang Y, et al. "Salusin-β mediate neuroprotective effects for Parkinson's disease." Biochem Biophys Res Commun, 2018;503(3):1428-1433. PMID: 30017195.
- [pubmed] Akyüz A, et al. "Relationship of serum salusin beta levels with coronary slow flow." Anatol J Cardiol, 2019;22(4):177-184. PMID: 31584433.
- [pubmed] Sipahi S, et al. "Relationship of salusin-alpha and salusin-beta levels with atherosclerosis in patients undergoing haemodialysis." Singapore Med J, 2019;60(4):210-215. PMID: 30311629.
- [pubmed] Wang Y, et al. "Salusin-β is superior to salusin-α as a marker for evaluating coronary atherosclerosis." J Int Med Res, 2020;48(2):300060520903868. PMID: 32054363.
- [pubmed] Wu LL, et al. "Salusin-β in Intermediate Dorsal Motor Nucleus of the Vagus Regulates Sympathetic-Parasympathetic Balance and Blood Pressure." Biomedicines, 2021;9(9). PMID: 34572305.
- [pubmed] Demir I, et al. "Intracerebroventricular salusin-β infusion to rats increases hypothalamus-pituitary-testicular axis hormones." Gen Comp Endocrinol, 2021;310:113820. PMID: 34015344.
- [pubmed] Alpsoy S, et al. "Assessment of salusin alpha and salusin beta levels in patients with newly diagnosed dipper and non-dipper hypertension." Clin Exp Hypertens, 2021;43(1):42-48. PMID: 32723189.
- [pubmed] Arkan A, et al. "The importance of circulating levels of salusin-α, salusin-β, and heregulin-β1 in atherosclerotic coronary arterial disease." Clin Biochem, 2021;87:19-25. PMID: 33031820.
- [pubmed] Argun D, et al. "Evaluation of salusin-α and salusin-β levels in patients with type 2 diabetes mellitus and determination of the impact of severity of hyperglycemia on salusin levels." Ir J Med Sci, 2021;190(4):1403-1411. PMID: 34109528.
- [pubmed] Karagöz A, et al. "A New Insight Into Pathophysiological Mechanism of Abdominal Aortic Aneurysm With Novel Parameters Salusin-β and Arterial Stiffness." Tex Heart Inst J, 2022;49(6). PMID: 36511944.
- [pubmed] Hajialilo M, et al. "Serum salusin-β levels in patients with systemic lupus erythematosus." Clin Rheumatol, 2023;42(8):2097-2103. PMID: 37120490.
- [pubmed] Albayrak B, et al. "Relationship between salusin beta levels and the severity of acute pancreatitis in patients." Medicine (Baltimore), 2024;103(25):e38685. PMID: 38905397.
- [pubmed] Medyńska A, et al. "Can Serum Salusin-α and Salusin-β Serve as Biomarkers for Early Atherosclerotic Lesions in Obese Children?." Int J Mol Sci, 2025;26(8). PMID: 40332043.
Sources & Citations
Every study on this page was read from its PubMed record on November 3, 2026. The sequence and precursor positions come from UniProt Q8N2E6; regulatory status comes from Drugs@FDA (openFDA), read the same day. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.