{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMyocardin (MYOCD) is recognized as a potent, tissue‐restricted transcriptional coactivator that associates with serum response factor (SRF) to drive the expression of muscle‐specific, contractile, and cyto‐structural genes that underlie cardiac and smooth muscle differentiation. Through precise interactions with CArG box–containing promoters, MYOCD programs the development of the smooth muscle cell (SMC) lineage and cardiomyocytes, as well as induces microRNAs (e.g., miR‑1) that further fine‐tune contractile protein expression and cytoskeletal organization. In addition, MYOCD’s partnership with SRF is essential for activating smooth muscle–specific genes and for maintaining the contractile phenotype, a function that is reinforced by its ability to modulate microRNA expression and to influence ion channel (e.g., KCNMB1) transcription."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the vascular context, MYOCD plays a central role in controlling phenotype modulation of vascular smooth muscle cells (VSMCs) and thereby influencing vascular tone, contractility, and remodeling. Aberrant MYOCD activity in cerebral VSMCs may trigger a hypercontractile state and impair amyloid‑β clearance in Alzheimer’s disease, while its interplay with signaling molecules such as STAT3 and transcriptional repressors (e.g., TEAD1) regulates the switch between a contractile and synthetic phenotype that is critical in atherosclerosis and other vascular hyperproliferative disorders. These studies illustrate that the balance of MYOCD activity is key to maintaining vascular homeostasis and that disruption of its regulatory network can contribute to cerebrovascular dysfunction and vascular disease progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "14"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its classical role in muscle differentiation, MYOCD has emerged as a critical modulator in diverse pathological settings including oncogenesis, fibrotic remodeling, and congenital disorders. Reduced MYOCD expression has been implicated in malignant transformation—where its restoration can drive differentiation and suppress proliferation in sarcomas and breast cancer cells—while its deregulation may promote epithelial–mesenchymal transition and metastasis in non–small cell lung cancer. Moreover, genetic variants and post‑translational modifications affecting MYOCD have been linked to developmental anomalies such as congenital megabladder and to altered cellular responses (e.g., via ERK1/2 phosphorylation or proteasomal turnover) that influence cell cycle progression, fibroblast–to–cardiomyocyte reprogramming, and cholesterol homeostasis in atherosclerosis. These findings underscore the pleiotropic roles of MYOCD and its integration into complex transcriptional and signaling networks."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "33"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kevin L Du, Hon S Ip, Jian Li, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Myocardin is sufficient for a smooth muscle-like contractile phenotype."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Arterioscler Thromb Vasc Biol (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1161/ATVBAHA.108.166066"}], "href": "https://doi.org/10.1161/ATVBAHA.108.166066"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18451334"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18451334"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Xiaochun Long, Darla L Tharp, Mary A Georger, et al. 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