ArticleBiochemical genetics2022
LncRNA-HOTAIR Inhibits H9c2 Apoptosis After Acute Myocardial Infarction via miR-206/FN1 Axis.
Article in Biochemical genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Identification of anoikis-related biomarkers linking immune infiltration to acute myocardial infarction.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Article
- Spotlight on HOX cluster‑embedded antisense lncRNAs in cardiovascular diseases (Review).International journal of molecular medicine · 2023Review
- The role and medical prospects of long non-coding RNAs in cardiovascular disease.Heart failure reviews · 2023Review
- Noncoding RNAs as Key Regulators for Cardiac Development and Cardiovascular Diseases.Journal of cardiovascular development and disease · 2023Review
- HOTAIR regulates SIRT3-mediated cardiomyocyte survival after myocardial ischemia/reperfusion by interacting with FUS.BMC cardiovascular disorders · 2023Article
- HOTAIR: a potential metastatic, drug-resistant and prognostic regulator of breast cancer.Molecular cancer · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although previous studies showed that long non-coding RNAs (lncRNAs) have critical roles in the pathogenesis of acute myocardial infarction (AMI), the underlying molecular mechanism that lncRNAs participate in MI remains unclear. Herein, we explored the expression of lncRNA HOX antisense non-coding RNA (HOTAIR) in the serum of MI patients and mouse model of AMI. Biological functions of HOTAIR in hypoxic H9c2 cells, the in vitro model of MI, were also assessed. RT-qPCR results showed that HOTAIR expression was downregulated in the serum of AMI patients and AMI mice. HOTAIR overexpression promoted H9c2 cell viability and inhibited cell apoptosis under hypoxic conditions. Mechanically, HOTAIR was regulated by miR-206 and FN1 was the direct target of miR-206. More importantly, miR-206 overexpression or FN1 knockdown reversed the effect of HOTAIR overexpression on H9c2 cell viability and apoptosis under hypoxic conditions. Therefore, targeting the HOTAIR/miR-206/FN1 axis may be a promising therapeutic method for MI.
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