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Updated: Jan 26, 2026
Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease
Published on: July 3, 2018
MicroRNA-133a and Myocardial Infarction
Yi Xiao1, Jiling Zhao1, Julian P Tuazon2
11 Department of Cardiology, Xiangya Hospital, Central South University, Changsha, PR China.
Abstract:
Myocardial infarction (MI) is the leading cause of morbidity and mortality in the world. The infarcted heart displays typical cell death cascades characterized by a loss of cells and fibrotic scarring in the myocardium. Cardiac hypertrophy and fibrosis largely contribute to ventricular wall thickening and stiffening, altogether defining an adverse cardiac remodeling that ultimately leads to impaired cardiac function and subsequent heart failure. Finding a strategy to promote therapeutic, instead of detrimental, cardiac remodeling may pose as a potent MI treatment. Accumulating evidence shows that microRNAs (miRNAs) may play an essential role in cardiovascular diseases. In particular, microRNA-133a (miR-133a) is one of the most abundant miRNAs in the heart. Multiple studies have demonstrated that miR-133a participates in the early pathology of MI, as well as in subsequent cardiac remodeling. In this review, we summarize recent research progress highlighting the regulatory effects of miR-133a in ischemic myocardial diseases, such as inhibiting angiogenesis, apoptosis, fibrosis, hypertrophy, and inflammation, while promoting therapeutic cardiac remodeling. The goal is to elicit a critical discussion on the translational direction of miRNA-mediated treatments towards a safe and effective MI therapy.
Insights
MicroRNA-133a (miR-133a) shows potential in treating myocardial infarction (MI) by inhibiting adverse cardiac remodeling. This research explores its role in promoting therapeutic repair after heart attack.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Regenerative Medicine
Background:
- Myocardial infarction (MI) is a leading global cause of death, characterized by cell death and fibrotic scarring.
- Adverse cardiac remodeling, including hypertrophy and fibrosis, leads to impaired heart function and heart failure.
- MicroRNAs (miRNAs) are increasingly recognized for their role in cardiovascular diseases.
Purpose of the Study:
- To review the regulatory effects of microRNA-133a (miR-133a) in ischemic myocardial diseases.
- To highlight miR-133a's role in promoting therapeutic cardiac remodeling after MI.
- To discuss the translational potential of miRNA-based therapies for MI.
Main Methods:
- Literature review of recent research on miR-133a and myocardial infarction.
- Analysis of studies detailing miR-133a's impact on cellular processes in the infarcted heart.
- Synthesis of evidence regarding miR-133a's therapeutic potential.
Main Results:
- miR-133a is abundant in the heart and plays a crucial role in MI pathology and remodeling.
- miR-133a has been shown to inhibit key detrimental processes including angiogenesis, apoptosis, fibrosis, hypertrophy, and inflammation.
- Evidence suggests miR-133a promotes beneficial cardiac repair mechanisms.
Conclusions:
- miR-133a demonstrates significant potential as a therapeutic agent for myocardial infarction.
- Targeting miR-133a may offer a novel strategy to mitigate adverse cardiac remodeling and improve outcomes.
- Further research is needed to translate miR-133a-based therapies into clinical practice for MI treatment.
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