{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nIn spinal cord injury models, miR‐1953 (also denoted as miR‐195-3p in related contexts) acts as a critical regulator of the PTEN/PI3K/AKT pathway. Specifically, the long non‐coding RNA ZFAS1 is upregulated following injury and functions as a molecular sponge for miR‐1953. This binding reduces the levels of available miR‐1953, which normally targets and suppresses PTEN, thereby leading to an increase in PTEN expression. The subsequent inactivation of the PI3K/AKT pathway is associated with enhanced cell apoptosis and inflammatory responses, contributing to the progression of spinal cord injury."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nConversely, in the context of myocardial infarction-induced cardiac fibrosis, miR‐195-3p is upregulated in response to injury and pro-fibrotic signals such as TGF-β1. Elevated miR‐195-3p levels promote fibrosis by targeting and reducing PTEN expression, thereby facilitating cardiac fibroblast activation, collagen deposition, and myofibroblast differentiation—a series of events that contribute to adverse cardiac remodeling and dysfunction following infarction. Inhibition of miR‐195-3p in these models restores PTEN expression and attenuates fibrotic processes, suggesting that modulation of this pathway may hold therapeutic promise for heart failure prevention."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yunxiang Chen, Zijian Wei, Jun Liu, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Long noncoding RNA ZFAS1 aggravates spinal cord injury by binding with miR-1953 and regulating the PTEN/PI3K/AKT pathway."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Neurochem Int (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.neuint.2021.104977"}], "href": "https://doi.org/10.1016/j.neuint.2021.104977"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "33524472"}], "href": "https://pubmed.ncbi.nlm.nih.gov/33524472"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Abdlay Carvalho, Zhenjun Ji, Rui Zhang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Inhibition of miR-195-3p protects against cardiac dysfunction and fibrosis after myocardial infarction."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Int J Cardiol (2023)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.ijcard.2023.131128"}], "href": "https://doi.org/10.1016/j.ijcard.2023.131128"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "37356730"}], "href": "https://pubmed.ncbi.nlm.nih.gov/37356730"}]}]}]}