About: Roles of MicroRNA-122 in Cardiovascular Fibrosis and Related Diseases

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About: Roles of MicroRNA-122 in Cardiovascular Fibrosis and Related Diseases Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Roles of MicroRNA-122 in Cardiovascular Fibrosis and Related Diseases
Creator	Liu, Ying Lin, Jian-Yu Zhong, Jiu-Chang Song, Jia-Wei Ran Miao, ·
Source	Medline; PMC
abstract	Fibrotic diseases cause annually more than 800,000 deaths worldwide, where of the majority accounts for cardiovascular fibrosis, which is characterized by endothelial dysfunction, myocardial stiffening and reduced dispensability. MicroRNAs (miRs), small noncoding RNAs, play critical roles in cardiovascular dysfunction and related disorders. Intriguingly, there is a critical link among miR-122, cardiovascular fibrosis, sirtuin 6 (SIRT6) and angiotensin-converting enzyme 2 (ACE2), which was recently identified as a coreceptor for SARS-CoV2 and a negative regulator of the rennin-angiotensin system. MiR-122 overexpression appears to exacerbate the angiotensin II-mediated loss of autophagy and increased inflammation, apoptosis, extracellular matrix deposition, cardiovascular fibrosis and dysfunction by modulating the SIRT6-Elabela-ACE2, LGR4-β-catenin, TGFβ-CTGF and PTEN-PI3K-Akt signaling pathways. More importantly, the inhibition of miR-122 has proautophagic, antioxidant, anti-inflammatory, anti-apoptotic and antifibrotic effects. Clinical and experimental studies clearly demonstrate that miR-122 functions as a crucial hallmark of fibrogenesis, cardiovascular injury and dysfunction. Additionally, the miR-122 level is related to the severity of hypertension, atherosclerosis, atrial fibrillation, acute myocardial infarction and heart failure, and miR-122 expression is a risk factor for these diseases. The miR-122 level has emerged as an early-warning biomarker cardiovascular fibrosis, and targeting miR-122 is a novel therapeutic approach against progression of cardiovascular dysfunction. Therefore, an increased understanding of the cardiovascular roles of miR-122 will help the development of effective interventions. This review summarizes the biogenesis of miR-122; regulatory effects and underlying mechanisms of miR-122 on cardiovascular fibrosis and related diseases; and its function as a potential specific biomarker for cardiovascular dysfunction.
has issue date	2020-08-27(xsd:dateTime)
bibo:doi	10.1007/s12012-020-09603-4
bibo:pmid	32856216
has license	no-cc
sha1sum (hex)	93436fd36a254a68ec3e2ecccd89fcb2f9141b20
schema:url	https://doi.org/10.1007/s12012-020-09603-4
resource representing a document's title	Roles of MicroRNA-122 in Cardiovascular Fibrosis and Related Diseases
has PubMed Central identifier	PMC7451782
has PubMed identifier	32856216
schema:publication	Cardiovasc Toxicol
resource representing a document's body	covid:93436fd36a254a68ec3e2ecccd89fcb2f9141b20#body_text
is schema:about of	named entity 'sirtuin' named entity 'overexpression' named entity 'MicroRNA' named entity 'Diseases' named entity 'CHARACTERIZED' named entity 'OVEREXPRESSION' named entity 'NEGATIVE REGULATOR' named entity 'ELABELA' named entity 'majority' named entity 'diseases' named entity 'SIRT6' named entity 'apoptosis' named entity 'MiR-122' named entity 'ACE2' named entity 'ACE2' named entity 'cardiovascular' named entity 'coreceptor' named entity 'negative regulator' named entity 'fibrosis' named entity 'cardiovascular' named entity 'angiotensin-converting enzyme 2' named entity 'SARS-CoV2' named entity 'angiotensin II' named entity 'cardiovascular dysfunction' named entity 'MicroRNA' named entity 'Fibrosis' named entity 'disorders' named entity 'autophagy' named entity 'cardiovascular dysfunction' named entity 'transfection' named entity 'FoxO3' named entity 'cellular migration' named entity 'fibrosis' named entity 'Ischemic cell death' named entity 'miR-122' named entity 'therapeutic target' named entity 'rat' named entity 'ultrastructural' named entity 'oxygen' named entity 'arrhythmia' named entity 'ROS' named entity 'molecular mechanisms' named entity 'miR-122' named entity 'cardiac remodeling' named entity 'arterial stiffening' named entity 'Bach' named entity 'miR-122' named entity 'Mice' named entity 'fibroblasts' named entity 'infarct' named entity 'vascular disease' named entity 'chronic inflammatory' named entity 'fibrosis' named entity 'cardiovascular mortality' named entity 'miR-122' named entity 'extracellular matrix' named entity 'pulmonary vascular' named entity 'TGFβ1' named entity 'mTOR' named entity 'apoptosis' named entity 'COVID-19' named entity 'reperfusion' named entity 'miR-122' named entity 'plasma' named entity 'mammalian target of rapamycin' named entity 'signaling pathway' named entity 'biomarker' named entity 'apoptosis' named entity 'miR-122' named entity 'epithelial' named entity 'inflammation' named entity 'FOXO3' named entity 'forkhead box' named entity 'atherosclerosis' named entity 'apelin' named entity 'miR-122' named entity 'cytoplasm'

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