Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
Open accessAbstract
Xiao-Jun Du, MBBS, PhD; Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases, Cardiovascular Research, , cvaf057, https://
AI snapshot
Written from the paper’s full text.
TL;DR
This editorial reviews the state of relaxin receptor (RXFP1)-targeted therapy for cardiovascular disease, prompted by a new study of the long-acting relaxin analogue AZD3427 in non-human primates with heart failure. It argues that the field is reviving after the RELAX-AHF failure, while flagging unresolved questions about chronic RXFP activation, mechanism, and delivery.
Key findings
The commentary highlights that AZD3427, an Fc-fused human relaxin with half-life extended to roughly 120 h, improved LVEF and stroke volume and lowered peripheral vascular resistance in aged non-human primates with HFrEF, with LVEF gains beginning at week 5 and continuing across 21 weeks of once-weekly subcutaneous dosing, then declining slowly over an 18-week washout. Unlike serelaxin in patients, AZD3427 produced no heart-rate increase and no improvement in the urinary albumin-to-creatinine ratio in this model. The author notes that the RELAX-AHF phase-III trial of serelaxin failed its primary endpoints of 6-month total and cardiovascular adverse events despite hemodynamic and biomarker benefits, and that relaxin as a peptide drug suffers from short action (<5 h), i.v. infusion requirement, nonlinear dose–response, and high production cost. He also points to ongoing development of oral small-molecule RXFP1 agonists, including AZD5462 (derived from ML290, itself found by screening 367,000 compounds), now in a 24-week phase IIb trial in stable chronic heart failure.
Methods
This is a narrative editorial/commentary, not an original study; it has no primary data, sample, or statistical analysis of its own. Its evidence base is the accompanying Papworth et al. paper on AZD3427 in non-human primates, the RELAX-AHF trial series and related serelaxin literature, a phase Ia/b first-in-human AZD3427 study, and prior reports on RXFP1 small-molecule agonists and relaxin fusion proteins/mRNA therapeutics. The author's assessment is organized around methodological strengths of the Papworth study (aged high-fat-diet NHP HFrEF model with comorbidities, randomized double-blind design, serial echocardiography, 18-week washout, ex vivo receptor pharmacology) and around gaps in knowledge of chronic RXFP activation.
Limitations
The author states that the reason for the slow onset and gradual loss of hemodynamic benefit with AZD3427 is unclear, possibly involving peripheral vascular resistance, ventricular performance, and pathological remodelling, and notes that myocardial tissue profiling was not performed. He also notes that the sustained rise in plasma renin with AZD3427 in HF animals is unexplained, and that differences from serelaxin results may stem from species, biological age, treatment duration, disease type, or differing RXFP signalling. Evident from the text itself: this is a single-author editorial without primary data, so its conclusions rest on interpretation of others' work; the comparison between AZD3427 in monkeys and serelaxin in patients is cross-species and cross-disease, and the author explicitly says the mechanisms of binding and activation by novel agonists, biased signalling, and long-term efficacy in HFpEF or acutely decompensated HF remain untested.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
20 of 42 cited sources checked · 11 supported · 0 flagged · accuracy not yet measured
- Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
The RELAX-AHF phase-III clinical trial failed to achieve its primary end-points of lowering 6-month total and cardiovascular adverse events.
“However, the RELAX -AHF phase-III clinical trial failed in achieving the primary end -points of lowering the 6-month total and cardiovascular adverse events, 3”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [3] Metra, 2019, . Effects of serelaxin in patients with acute heart failure, N Engl J Med source
The Primary and Key Secondary End Points section reports that RELAX-AHF-2 did not significantly reduce cardiovascular death at 180 days and that death from any cause was similar between groups. But the claim names RELAX-AHF rather than RELAX-AHF-2 and calls both six-month outcomes primary end points; the Primary and Secondary End Points section identifies all-cause death as secondary and worsening heart failure at 5 days as the other primary end point. The indexed passages provide no page number. (LLM, conf=0.88)
Experimental — accuracy not yet measured
- Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
AZD3427 was developed by fusion of the human IgG Fc portion to human relaxin.
“AZD3427 was developed by the fusion of human IgG Fc portion to human relaxin.7”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [7] Connolly, 2024, Novel relaxin receptor RXFP1 agonist AZD3427 in the treatment of heart failure: a phase 1a/b, first-in-human, randomized, single-blind, placebo-controlled study, J Am Heart Assoc source
The introductory passage under Abstract > Registration describes AZD3427 as a fusion protein containing the Fc portion of human IgG1. It says that portion is linked to a peptide sequence derived from human relaxin, not to human relaxin itself. (LLM, conf=0.85)
Experimental — accuracy not yet measured
- Premisecitation
LVEF exhibited a slow and progressive decline during the 18-week washout period towards the pre-treatment baseline.
“Likewise, LVEF exhibited a slow and progressive decline during the 18-week washout period towards the pre-treatment baseline.6”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [6] Papworth, 2025, A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction, Cardiovasc Res source
- Study design and conductcitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
The study was a randomized and double-blind drug trial.
“this study was a randomized and double-blind drug trial.”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [6] Papworth, 2025, A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction, Cardiovasc Res source
Methods, ‘NHP study cohort and design,’ says the non-human primates were randomized to vehicle or AZD3427 treatment groups. Methods, ‘Imaging and HDO,’ says assessors were blinded to treatment assignment, but does not establish that the study was double-blind. (LLM, conf=0.90)
Experimental — accuracy not yet measured
- Premisecitation
Papworth et al found no evidence for heart rate increment by AZD3427 treatment in the NHP model.
“Papworth et al found no evidence for either heart rate increment or improvement of renal parameter urinary albumin creatinine ratio (UACR) by AZD3427 treatment in the NHP model.6”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [6] Papworth, 2025, A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction, Cardiovasc Res source
- Premisecitation
A recent phase Ia/b study on AZD3427 in HF patients showed trends toward improvement of SV and eGFR at the end of a 5-week treatment period.
“aligning with a recent phase Ia/b study on AZD3427 in HF patients that showed trends toward improvement of SV and eGFR at the end of a 5-week treatment period.7”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [7] Connolly, 2024, Novel relaxin receptor RXFP1 agonist AZD3427 in the treatment of heart failure: a phase 1a/b, first-in-human, randomized, single-blind, placebo-controlled study, J Am Heart Assoc source
- Premisereasoning§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
AZD3427 has reduced renal clearance.
“With increased molecular size, the renal clearance of AZD3427 is reduced”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [7] Connolly, 2024, Novel relaxin receptor RXFP1 agonist AZD3427 in the treatment of heart failure: a phase 1a/b, first-in-human, randomized, single-blind, placebo-controlled study, J Am Heart Assoc source
The Results pharmacokinetics sections report AZD3427’s terminal half-life, but do not identify renal clearance or increased molecular size as its cause. The reported increase in estimated glomerular filtration rate concerns patients’ kidney function, not clearance of AZD3427. Searches for molecular size and renal clearance found no passage supporting the claim; page numbers were unavailable. (LLM, conf=0.76)
Experimental — accuracy not yet measured
- Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
Papworth et al reported a therapeutic effect of AZD3427 in a non-human primate model of HFrEF.
“Papworth et al reported on the therapeutic effect of a novel long-acting relaxin analogue AZD3427 in a non-human primate (NHP) model of HF with reduced left ventricular ejection fraction (LVEF).6”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [6] Papworth, 2025, A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction, Cardiovasc Res source
- Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
AZD3427 has preserved molecular stability.
“with preserved molecular stability.”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [7] Connolly, 2024, Novel relaxin receptor RXFP1 agonist AZD3427 in the treatment of heart failure: a phase 1a/b, first-in-human, randomized, single-blind, placebo-controlled study, J Am Heart Assoc source
The Results pharmacokinetics passages (Parts A and B; page not provided) report AZD3427 serum concentrations and terminal half-life, but do not assess whether its molecular structure remains stable. Searches for molecular stability, degradation, and the claim’s wording found no passage addressing that property. (LLM, conf=0.76)
Experimental — accuracy not yet measured
- Premisereasoning§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
AZD3427 has a half-life prolonged to approximately 120 h.
“its half-life prolonged to approximately 120 h”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [7] Connolly, 2024, Novel relaxin receptor RXFP1 agonist AZD3427 in the treatment of heart failure: a phase 1a/b, first-in-human, randomized, single-blind, placebo-controlled study, J Am Heart Assoc source
The Results (Part A, Pharmacokinetics) report a terminal half-life of 117 hours—approximately 120 hours—after a single intravenous dose in healthy volunteers. The claim omits that condition: the same section reports 162–214 hours after subcutaneous dosing, while Part B reports 315–325 hours after weekly dosing in patients with heart failure. (LLM, conf=0.88)
Experimental — accuracy not yet measured
- Premisecitation
AZD3427 treatment significantly improves LVEF in monkeys.
“The significant improvement in LVEF and stroke volume (SV), together with reduction in the peripheral vascular resistance in AZD3427-treated monkeys is convincing”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [6] Papworth, 2025, A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction, Cardiovasc Res source
- Premisecitation
AZD3427 treatment significantly improves stroke volume in monkeys.
“The significant improvement in LVEF and stroke volume (SV), together with reduction in the peripheral vascular resistance in AZD3427-treated monkeys is convincing”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [6] Papworth, 2025, A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction, Cardiovasc Res source
The Results section (page unavailable) reports a notable increase in stroke volume in AZD3427-treated monkeys with cardiac dysfunction. It explicitly calls the improvement in ejection fraction significant, but does not establish statistical significance for stroke volume, as the claim does. (LLM, conf=0.84)
Experimental — accuracy not yet measured
- Premisecitation
AZD3427 treatment reduces peripheral vascular resistance in monkeys.
“The significant improvement in LVEF and stroke volume (SV), together with reduction in the peripheral vascular resistance in AZD3427-treated monkeys is convincing”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [6] Papworth, 2025, A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction, Cardiovasc Res source
- Premisecitation
Papworth et al found no evidence for improvement of renal parameter UACR by AZD3427 treatment in the NHP model.
“Papworth et al found no evidence for either heart rate increment or improvement of renal parameter urinary albumin creatinine ratio (UACR) by AZD3427 treatment in the NHP model.6”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [6] Papworth, 2025, A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction, Cardiovasc Res source
- Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
The pleiotropic signaling mechanisms utilized by RXFP form the basis for its favourable effectiveness in cardiovascular disease.
“The pleiotropic signaling mechanisms utilized by RXFP form the basis for its favourable effectiveness in the setting of cardiovascular disease.1,2”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation
Animal studies reported heart rate increment following administration of serelaxin or relaxin due to RXFP coupling to stimulatory G-protein.
“Animal studies reported heart rate increment following administration of serelaxin or relaxin due to RXFP coupling to stimulatory G-protein.1,2”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
Relaxin as a peptide drug is short-acting (<5 h).
“including its short -acting (<5 h), requirement of i.v.infusion, complex and nonlinear dose-effect relationship, and high cost of production.1,2”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
Relaxin as a peptide drug has a complex and nonlinear dose-effect relationship.
“complex and nonlinear dose-effect relationship”
Quote in the paperNot a substantial claim0 of 2 sources checked - Interpretationreasoning§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
Enthusiasm for using relaxin to treat HF patients has declined since the RELAX-AHF trial.
“The enthusiasm for using relaxin to treat HF patients has declined since then.”
Quote in the paperSubstantial claim - Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
Relaxin as a peptide drug requires i.v. infusion.
“requirement of i.v.infusion”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseases
Relaxin as a peptide drug has high production cost.
“high cost of production.1,2”
Quote in the paperNot a substantial claim0 of 2 sources checked - Premisecitation
Preclinical relaxin studies have revealed anti-inflammatory and anti-fibrotic actions.
“Preclinical relaxin studies have revealed anti-inflammatory and anti-fibrotic actions, 1,2”
Quote in the paperSubstantial claim0 of 2 sources checked
- May combine two claims. 10
- Classified as probably not a substantial claim. 2
May combine two claims.
Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseasesDespite the RELAX-AHF trial failure, clinical benefits in haemodynamics and biomarker profile were demonstrated.
“despite the demonstration of clinical benefits in haemodynamics and biomarker profile.4,5”
Quote in the paperSubstantial claim2 of 2 sources checked- cites [4] Teerlink, 2020, Effects of serelaxin in patients admitted for acute heart failure: a meta-analysis, Eur J Heart Fail source
- cites [5] Grand, 2022, Blood pressure drops during hospitalization for acute heart failure treated with serelaxin: a patient-level analysis of 4 randomized controlled trials, Circ Heart Fail source
The Conclusions (page unavailable) say that blood-pressure drops appeared less harmful in patients treated with serelaxin than in those receiving usual care or placebo, providing limited support for a haemodynamic benefit. The paper does not demonstrate a benefit in biomarker profile; it uses NT-proBNP in its analyses but does not report an improvement in it with serelaxin. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductcitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseasesThe study included an 18-week washout observation, which is helpful to confirm the efficacy of AZD3427.
“the authors astutely included an 18-week period of washout observation, which is helpful to confirm the efficacy of AZD3427.”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [6] Papworth, 2025, A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction, Cardiovasc Res source
May combine two claims.
PremisecitationPapworth et al showed improvement in LVEF starting from week-5 and progressively further improving throughout the 21-week treatment without a sign of reaching a plateau.
“Papworth et al clearly showed improvement in LVEF starting from week-5 and progressively further improving throughout the 21-week period of treatment without a sign of reaching a plateau.6”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [6] Papworth, 2025, A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction, Cardiovasc Res source
The Results (page unavailable) report improved ejection fraction in treated non-human primates at 21 weeks, and the Discussion says EF had not reached a pharmacodynamic steady state by then, supporting the no-plateau point. The Methods list an assessment at Week 5, but our copy does not state that improvement began then or that EF increased progressively at every assessment through Week 21. (LLM, conf=0.86)
Experimental — accuracy not yet measured
May combine two claims.
PremisecitationA NIH team identified two lead hits following screening of 367,000 compounds, including a lead ML290, from which a derivative AZD5462 was obtained.
“a NIH team identified two lead hits following meticulous screening of 367,000 compounds, 9 including a lead ML290, from which a derivative AZD5462 was obtained (Figure ). 10”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites [9] Chen, 2013, Identification of small-molecule agonists of human relaxin family receptor 1 (RXFP1) by using a homogenous cell-based cAMP assay, J Biomol Screen source
- cites [10] Granberg, 2024, Discovery of clinical candidate AZD5462, a celective oral allosteric RXFP1 agonist for treatment of heart failure, J Med Chem source
May combine two claims.
Study design and conductcitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseasesA HFrEF model was developed in aged NHPs by 2-year high-fat-diet feeding, leading to phenotypes simulating clinical conditions, including LV systolic dysfunction and comorbidities (obesity, dyslipidaemia, early signs of hypertension and diabetes).
“a HFrEF model was developed in aged NHPs by 2-year high-fat-diet feeding, leading to phenotypes simulating clinical conditions, including LV systolic dysfunction and presence of comorbidities (e.g.obesity, dyslipidaemia, and early signs of hypertension and diabetes).”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [6] Papworth, 2025, A novel long-acting relaxin-2 fusion, AZD3427, improves cardiac performance in non-human primates with cardiac dysfunction, Cardiovasc Res source
May combine two claims.
Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseasesRelaxin is a peptide hormone that binds primarily to RXFP1 and initiates complex signaling.
“Relaxin is a peptide hormone that binds to the G protein-coupled relaxin family peptide receptor (RXFP), primarily RXFP1, initiating complex signaling.1,2”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
Premisecitation§ Revivifying research on relaxin receptor-targeted therapy for cardiovascular diseasesPreclinical data suggest relaxin has beneficial cardiovascular effects, including lowering peripheral vascular resistance, improving renal function, and antagonizing fibrosis, inflammation, and ischemic injury.
“Abundant preclinical data suggest beneficial cardiovascular effects of relaxin including lowering peripheral vascular resistance, improving renal function and antagonizing fibrosis, inflammation and ischemic injury.”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationAccording to the RELAX-AHF study, infusion with serelaxin (48 hours) induced rapid onset (from day-2) of favourable effects in biomarker profiles, hemodynamics (e.g. reduction in perivascular resistance, modest increase in heart rate) and renal function (estimated by creatinine or eGFR).
“According to the RELAX-AHF study, infusion with serelaxin (48 hours) induced rapid onset (from day-2) of favourable effects in biomarker profiles, hemodynamics (e.g.reduction in perivascular resistance, modest increase in heart rate) and renal function (estimated by creatinine or eGFR).[3][4][5]”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [3][4][5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S2 (checkable). May combine two claims.
InterpretationreasoningPapworth et al present an important piece of translational research with the findings supporting further clinical development of AZD3427 for HF therapy.
“Papwerth et al present an important piece of translational research with the findings supporting further clinical development of AZD3427 for HF therapy.”
Quote in the paperNot a substantial claim- Rests on an assumption: The beneficial effects of AZD3427 in the NHP HFrEF model predict clinical benefit in human HF patients.
May combine two claims.
PremisecitationFull activation of RXFP requires relaxin binding at both the ectodomain and the transmembrane loop, and the presence of the LDLa domain.
“Full activation of RXFP requires relaxin binding at both the ectodomain and the transmembrane loop, and the presence of the LDLa domain (Figure ).1,2”
Quote in the paperSubstantial claim0 of 2 sources checked
The paper relies on this without support.
The beneficial effects of AZD3427 in the NHP HFrEF model predict clinical benefit in human HF patients.
“Papwerth et al present an important piece of translational research with the findings supporting further clinical development of AZD3427 for HF therapy.”
Cites
Relaxin family peptides and their receptors
Bathgate, R. A. D., Halls, M. L., van der Westhuizen, E. T., Callander, G. E., Kocan, M., & Summers, R. J. (2013) · Physiological Reviews · doi:10.1152/physrev.00001.2012 · Cited by 534 · see citing works
. Effects of serelaxin in patients with acute heart failure
Metra, M., Teerlink, J. R., Cotter, G., Davison, B. A., Felker, G. M., Filippatos, G., Greenberg, B. H., Pang, P. S., Ponikowski, P., Voors, A. A., et al. (2019) · New England Journal of Medicine · doi:10.1056/nejmoa1801291 · Cited by 282 · see citing works
Cardiovascular effects of relaxin: from basic science to clinical therapy
Du, X.-J., Bathgate, R. A. D., Samuel, C. S., Dart, A. M., & Summers, R. J. (2010) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2009.198 · Cited by 188 · see citing works
Self-citationEffects of serelaxin in patients admitted for acute heart failure: a meta-analysis
Teerlink, J. R., Davison, B. A., Cotter, G., Maggioni, A. P., Sato, N., Chioncel, O., Ertl, G., Felker, G. M., Filippatos, G., Greenberg, B. H., et al. (2020) · European Journal of Heart Failure · doi:10.1002/ejhf.1692 · Cited by 41 · see citing works
Chen, C. Z., Southall, N., Xiao, J., Marugan, J. J., Ferrer, M., Hu, X., Jones, R. E., Feng, S., Agoulnik, I. U., Zheng, W., et al. (2013) · SLAS Discovery · doi:10.1177/1087057112469406 · Cited by 31 · see citing works
Mallart, S., Ingenito, R., Bianchi, E., Bresciani, A., Esposito, S., Gallo, M., Magotti, P., Monteagudo, E., Orsatti, L., Roversi, D., et al. (2021) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.0c01533 · Cited by 29 · see citing works
Granberg, K. L., Sakamaki, S., Larsson, N., Bergström, F., Fuchigami, R., Niwa, Y., Ryberg, E., Backmark, A., Kato, H., Miyazaki, S., et al. (2024) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.3c02184 · Cited by 26 · see citing works
Connolly, K., George, R., Omar, S., Matsson, E., Åstrand, M., Althage, M., Pettersen, D., Mohamed, E., Fang, K., Lima, J. A. C., et al. (2024) · Journal of the American Heart Association · doi:10.1161/jaha.123.034067 · Cited by 13 · see citing works
Papworth, M., Kulkarni, S., Antonsson, M., Sermadiras, I., Hovdal, D., Connolly, K., Olsson, J., Shukla, A., Cotton, P., Althage, M., et al. (2025) · Cardiovascular Research · doi:10.1093/cvr/cvaf031 · Cited by 8 · see citing works
Grand, J., Miger, K., Sajadieh, A., Køber, L., Torp-Pedersen, C., Ertl, G., López-Sendón, J., Pietro Maggioni, A., Teerlink, J. R., Sato, N., et al. (2022) · Circulation: Heart Failure · doi:10.1161/circheartfailure.121.009199 · Cited by 6 · see citing works
Flagged first, then by citations
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Borlaug, B. A., Testani, J. M., Petrie, M. C., Wang, Z., Cunningham, J. W., Adams, K. F., Amir, O., Bělohlávek, J., Bocchi, E. A., Freitas, A. F., et al. (2025) · Nature Medicine · doi:10.1038/s41591-025-03939-6 · Cited by 15 · see citing works
- Authors
- Du, X.-J.
- Affiliations
- Baker Heart and Diabetes Institute (AU)
- Corresponding author
- Du, Xiao-Jun
- ORCID
- Du, Xiao-Jun
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2025-04-17
- Volume
- 121
- Issue
- 6
- Pages
- 836-838
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- OpenAlex
- W4409556966
- Cited by
- 1
- References
- 10
- Citations by year
- 2025: 1
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cardiovascular Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- NHMRC of Australia
- Nature Science Fund of China
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Pregnancy-related medical research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Pharmacology › Apelin-related biomedical research
- Keywords
- relaxin receptor, cardiovascular disease, relaxin, cardiovascular pharmacology
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