ArticleAging2021
Constitutive activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway in mice with myocardial injury following acute myocardial infarction.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- NEAT1 Coordinates a PDLIM5-CACNA1C Regulatory Program Associated with a Potentially Arrhythmogenic Cardiomyocyte State in the Border Zone During Early Myocardial Infarction.International journal of molecular sciences · 2026Article
- NEAT1 regulates VSMC differentiation and calcification in as long noncoding RNA NEAT1 enhances phenotypic and osteogenic switching of vascular smooth muscle cells in atherosclerosis via scaffolding EZH2.American journal of physiology. Cell physiology · 2024Article
- The roles of long noncoding RNA NEAT1 in cardiovascular diseases.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- LncRNA-IMAT1 Promotes Invasion of Meningiomas by Suppressing KLF4/hsa-miR22-3p/Snai1 Pathway.Molecules and cells · 2022Article
- Network Pharmacology-Based Combined with Experimental Validation Study to Explore the Underlying Mechanism ofDrug design, development and therapy · 2022Article
- Review
- The Regulation Mechanisms and Clinical Application of MicroRNAs in Myocardial Infarction: A Review of the Recent 5 Years.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronary heart disease (CHD) with myocardial infarction (MI) being the manifestation of its advanced manifestation, remains the primary cause of mortality and disability worldwide. Aberrant expression of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) can affect the occurrence of MI in CHD. The present study aimed to explore whether NEAT1 sponging with miR-22-3p affected MI in CHD and its related mechanism. We established that the NEAT1 and Ltb4r1 expressions were increased, while miR-22-3p expression was down-regulated in MI mice following CHD. NEAT1 could competitively bind to miR-22-3p and positively regulate Ltb4r1 expression. Ltb4r1 was the downstream target of miR-22-3p. Moreover, silencing NEAT1 or downregulating Ltb4rl expression resulted in improved cardiac function, reduced infarct size, and declined levels of IL-1β, IL-6, and IL-18. Furthermore, silencing of NEAT1 also inhibited apoptosis by decreasing levels of Cleaved caspase-3 and Bax, and increasing Bcl-2 level through sponging miR-22-3p, resulting in reduced myocardial injury in CHD. Altogether, the activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway appears to aggravate myocardial injury following a MI, which suggested that this signaling may be a useful target for improved and more individualized treatments for MI.
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