Обзорная статья

Role of miRNA and lncRNAs in organ fibrosis and aging

Soudeh Ghafouri‐FardDepartment of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, IranAtefe AbakPhytochemistry Research Center, Shahid Beheshti University of Medical Sciences, Tehran, IranSeyedeh Fahimeh TalebiDepartment of Pharmacology, Birjand University of Medical Sciences, Birjand, IranHamed ShooreiDepartment of Anatomical Sciences, Faculty of Medicine, Birjand University of Medical Sciences, Birjand, IranWojciech BranickiMalopolska Centre of Biotechnology, Jagiellonian University, Krakow, Poland. Electronic address: [email protected]Mohammad TaheriUrology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: [email protected]Nader Akbari DilmaghaniSkull Base Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Electronic address: [email protected]

2021en

ABI

Аннотация

Fibrosis is the endpoint of pathological remodeling. This process contributes to the pathogenesis of several chronic disorders and aging-associated organ damage. Different molecular cascades contribute to this process. TGF-β, WNT, and YAP/TAZ signaling pathways have prominent roles in this process. A number of long non-coding RNAs and microRNAs have been found to regulate organ fibrosis through modulation of the activity of related signaling pathways. miR-144-3p, miR-451, miR-200b, and miR-328 are among microRNAs that participate in the pathology of cardiac fibrosis. Meanwhile, miR-34a, miR-17-5p, miR-122, miR-146a, and miR-350 contribute to liver fibrosis in different situations. PVT1, MALAT1, GAS5, NRON, PFL, MIAT, HULC, ANRIL, and H19 are among long non-coding RNAs that participate in organ fibrosis. We review the impact of long non-coding RNAs and microRNAs in organ fibrosis and aging-related pathologies.

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Идентификаторы

DOI: 10.1016/j.biopha.2021.112132

Цитирования и источники

Цитирований: 2Использованных источников: 0

Показатели — AkademScholar