ArticleHuman cell2021
MiR-100-5p regulates cardiac hypertrophy through activation of autophagy by targeting mTOR.
Article in Human cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- MiR-100-5p is involved in severe pneumonia in children by targeting MTOR.BMC immunology · 2026Article
- MiR-107 as a Biomarker Predicts Cardiac Hypertrophy in Chronic Hemodialysis Patients.Anatolian journal of cardiology · 2025Article
- Human Neural Progenitor Cell-Derived Exosomes Deliver miR- 100 - 5p Targeting NOX4 mRNA to Alleviate Oxidative Stress in Acute Ischemia Injury.Molecular neurobiology · 2025Article
- NAT10 Mediates Cardiac Fibrosis Induced by Myocardial Infarction Through ac4C Modification of TGFBR1 mRNA.Cell biology and toxicology · 2025Article
- Role and potential mechanisms of miR‑100 in different diseases (Review).Oncology reports · 2025Review
- MicroRNA-100-5p Exacerbates Myocardial Ischemia-Reperfusion Injury Through Downregulation of PRMT5.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- miR‑100: A key tumor suppressor regulatory factor in human malignant tumors (Review).International journal of molecular medicine · 2025Review
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- Macrophage-derived mir-100-5p orchestrates synovial proliferation and inflammation in rheumatoid arthritis through mTOR signaling.Journal of nanobiotechnology · 2024Article
- Oral SpirocheteInternational journal of molecular sciences · 2023Article
- Recent Advances in Extracellular Vesicles in Amyotrophic Lateral Sclerosis and Emergent Perspectives.Cells · 2023Review
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- Progress and Challenges of Understanding Cardiorenal Syndrome Type 3.Reviews in cardiovascular medicine · 2023Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Autophagy has been proved to play a vital role in cardiac hypertrophy. The present study was designed to investigate the relationship between miR-100-5p and autophagy in the development of cardiac hypertrophy. Here, miR-100-5p expression was detected in abdominal aortic coarctation (AAC)-induced cardiac hypertrophy rats and Angiotensin II (Ang II)-stimulated cardiomyocytes. In vitro and in vivo experiments were performed to explore the function of miR-100-5p on autophagy and cardiac hypertrophy. We also investigated the mechanism of miR-100-5p on autophagy with dual-luciferase reporter assays, RNA immunoprecipitation (RIP), quantitative real-time PCR (qRT-PCR), western blot, immunofluorescence, and transmission electron microscopy (TEM). The results showed that miR-100-5p was highly expressed in hypertrophic hearts and Ang II-induced cardiomyocytes. Overexpression of miR-100-5p promoted the expression of cardiac hypertrophy markers ANP, BNP and β-MHC and cell surface area, while those were suppressed by miR-100-5p inhibitor. Knockdown of miR-100-5p by antagomiR significantly improves cardiac function and attenuate cardiac hypertrophy in vivo. Mechanistic investigation has found that miR-100-5p promote autophagy by targeting mTOR. Inhibition of autophagy by 3-methyladenine (3-MA) or mTOR overexpression could reverse the function of miR-100-5p in cardiac hypertrophy. These results elucidate that miR-100-5p promoted the pathogenesis of cardiac hypertrophy through autophagy activation by targeting mTOR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.