{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nHuman relaxin‐2 (RLN2) is emerging as a potent antifibrotic and matrix‐modulating hormone. In cardiac, renal, and hepatic tissues, RLN2 has been shown to normalize collagen levels, inhibit myofibroblast differentiation, and attenuate extracellular matrix production by interfering with transforming growth factor–β (TGF‐β)–mediated signaling. In preclinical models of hypertension and diabetic nephropathy, RLN2 reduced oxidative stress, increased nitric oxide bioavailability, and restored matrix metalloproteinase (MMP) balance by reducing profibrotic mediators and enhancing collagen-degrading enzymes. These actions contribute to improvements in cardiac performance, renal function, and the prevention of tissue fibrosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nRLN2 also plays diverse roles in cancer biology, where its expression and signaling elicit complex and sometimes paradoxical effects. In prostate, thyroid, and other cancers, increased RLN2 levels have been associated with enhanced tumor cell invasiveness, anchorage-independent growth, and angiogenesis through the activation of signaling pathways such as phosphoinositide 3-kinase/Akt, cyclic adenosine monophosphate/protein kinase A (cAMP/PKA), and nuclear factor–κB. In some models, RLN2 facilitates androgen receptor activation via β-catenin stabilization, whereas in others it modulates extracellular protease production to promote cell motility. Collectively, these findings suggest that RLN2 can act as an autocrine/paracrine factor to drive cancer progression and metastasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in fibrosis and tumor biology, RLN2 is a multifunctional hormone that regulates reproductive tissues and vascular as well as neural systems. In models of early pregnancy, RLN2 stimulates uterine growth, enhances endometrial angiogenesis, and modulates MMP activity to maintain tissue integrity. Its binding to specific G-protein–coupled receptors (RXFP1 and RXFP2) involves complex structure–activity relationships including negative cooperativity, dimerization, and signal switching that fine-tune its cellular actions. In addition, RLN2 influences extracellular matrix remodeling in ligamentous tissues and contributes to cardiovascular and central nervous system regulation via pathways such as PI3K/Akt and nitric oxide signaling. These diverse receptor-mediated actions have been detailed in structural, receptor binding, and gene regulatory studies, highlighting RLN2’s potential as a therapeutic modulator in reproductive disorders, ligament remodeling, and cardiovascular diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Edna D Lekgabe, Helen Kiriazis, Chongxin Zhao, et al. 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