Relaxin-2 as a Potential Biomarker in Cardiovascular Diseases

Abstract

The pleiotropic hormone relaxin-2 plays a pivotal role in the physiology and pathology of the cardiovascular system. Relaxin-2 exerts relevant regulatory functions in cardiovascular tissues through the specific receptor relaxin family peptide receptor 1 (RXFP1) in the regulation of cardiac metabolism; the induction of vasodilatation; the reversion of fibrosis and hypertrophy; the reduction of inflammation, oxidative stress, and apoptosis; and the stimulation of angiogenesis, with inotropic and chronotropic effects as well. Recent preclinical and clinical outcomes have encouraged the potential use of relaxin-2 (or its recombinant form, known as serelaxin) as a therapeutic strategy during cardiac injury and/or in patients suffering from different cardiovascular disarrangements, especially heart failure. Furthermore, relaxin-2 has been proposed as a promising biomarker of cardiovascular health and disease. In this review, we emphasize the relevance of the endogenous hormone relaxin-2 as a useful diagnostic biomarker in different backgrounds of cardiovascular pathology, such as heart failure, atrial fibrillation, myocardial infarction, ischemic heart disease, aortic valve disease, hypertension, and atherosclerosis, which could be relevant in daily clinical practice and could contribute to comprehending the specific role of relaxin-2 in cardiovascular diseases.

Antihypertensive effect and mechanism of the traditional recipe of medicine food homology (Buyang Huanwu Decoction) in China: Meta analysis and network pharmacological exploration

“…Excessive, calcium intake can regulate blood pressure by affecting the renin-angiotensin-aldosterone system (RAAS) [ 67 ]. Relaxin inhibits vasoconstrictive substances such as ET-1 and Ang II, while increasing vascular endothelial MMP activity that produces vasodilatory effects by degrading ET-1 released from endothelial cells, activating endothelin B-type receptors, and inducing the endothelial release of NO [ 68 ]. Relaxin may also improve hypertension-induced endothelial dysfunction by increasing NO-dependent relaxation and decreasing endothelium-dependent contractions [ 69 ].…”

The influence of embryo stage on obstetric complications and perinatal outcomes following programmed compared to natural frozen-thawed embryo transfer cycles: A systematic review and meta-analysis

“…Relaxin, a 6-kDa peptide, is probably a potential mediator [16]. It is predominantly secreted by CL granulosa lutein cells in the late luteal phase (50-100 pg/ml) and reaches a peak concentration of 1000-2500 pg/mL in the rst trimester when pregnancy occurs [17]. Circulating relaxin was undetectable in women lacking CL [18][19].…”

The influence of embryo stage on obstetric complications and perinatal outcomes following programmed compared to natural frozen-thawed embryo transfer cycles: a systematic review and meta-analysis

“…Relaxin, a 6-kDa peptide, is probably a potential mediator ( 38 ). It is predominantly secreted by CL granulosa lutein cells in the late luteal phase (50-100 pg/ml) and reaches a peak concentration of 1000-2500 pg/mL in the first trimester when pregnancy occurs ( 39 ). Circulating relaxin was undetectable in women lacking CL ( 40 , 41 ).…”