{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNR3C2, which encodes the mineralocorticoid receptor (MR), plays a pivotal role in cardiovascular and renal homeostasis. In vascular smooth muscle and endothelial cells, MR is activated by aldosterone to regulate a specific gene program that influences vascular inflammation, fibrosis, calcification, and remodeling—processes central to the development of ischemic cardiovascular events and salt‐sensitive hypertension. In the myocardium and kidney, MR activation contributes to pathological remodeling and arrhythmogenesis, while distinct post‐translational modifications (such as phosphorylation at S843) fine‐tune its ligand binding and tissue‐specific actions. Moreover, studies employing conditional overexpression of MR in endothelial and cardiomyocyte models underscore its direct contribution to increased vascular contractility, oxidative stress, and blood pressure dysregulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, extensive structural and biochemical analyses have clarified the mechanisms by which NR3C2 confers ligand specificity. Detailed crystallographic studies reveal that aldosterone’s potency arises from an intricate hydrogen‐bond network involving residues such as Asn770 and Thr945, while naturally occurring mutations (e.g., S810L) can switch classical antagonists like progesterone into potent agonists. Furthermore, investigations into coactivator recruitment demonstrate that ligand binding induces distinct conformational changes in the receptor’s ligand‐binding domain, a process that can be modulated by factors including Rac1 and by novel nonsteroidal antagonists (such as CS‑3150), which selectively disrupt MR signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its classical roles in salt and water balance, NR3C2 has emerged as a key regulator in central stress responses, mood, metabolism, and even tumor suppression. In the brain, MR mediates the actions of glucocorticoids on cognitive functions, emotional regulation, and the feedback control of the hypothalamic–pituitary–adrenal axis—with genetic variants influencing cortisol dynamics and depression risk. In peripheral tissues such as adipose and pancreatic epithelia, MR functions extend to modulating inflammatory responses, adipogenesis, and epithelial–mesenchymal transition, with reduced expression linked to more aggressive cancers. Developmental studies further reveal that NR3C2 expression is tightly regulated in the neonatal kidney, contributing to the transient aldosterone resistance observed in early life, while polymorphisms in the NR3C2 gene also affect blood pressure responses and aldosterone levels in the general population."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Iris Z Jaffe, Michael E Mendelsohn "}, {"type": "b", "children": [{"type": "t", "text": "Angiotensin II and aldosterone regulate gene transcription via functional mineralocortocoid receptors in human coronary artery smooth muscle cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Circ Res (2005)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1161/01.RES.0000159937.05502.d1"}], "href": "https://doi.org/10.1161/01.RES.0000159937.05502.d1"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "15718497"}], "href": "https://pubmed.ncbi.nlm.nih.gov/15718497"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Antoine Ouvrard-Pascaud, Yannis Sainte-Marie, Jean-Pierre Bénitah, et al. 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