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Isolation, Transfection, and Long-Term Culture of Adult Mouse and Rat Cardiomyocytes
Published on: October 10, 2020
Reviewing the Limitations of Adult Mammalian Cardiac Regeneration: Noncoding RNAs as Regulators of Cardiomyogenesis
Robin Verjans1, Marc van Bilsen2, Blanche Schroen1
1Department of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, 6200 MD Maastricht, the Netherlands.
Insights
Adult hearts cannot regenerate due to limited cardiomyocyte division. Understanding noncoding RNAs like microRNAs and long noncoding RNAs is key to unlocking cardiac regeneration potential for treating heart failure.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Regenerative Medicine
Background:
- The adult mammalian heart has a limited capacity for regeneration after injury, often leading to heart failure.
- Cardiomyocyte proliferation is a significant barrier to cardiac repair, though limited self-renewal and regeneration occur early post-birth.
- Understanding the molecular mechanisms governing cardiomyocyte division is crucial for developing therapeutic strategies.
Purpose of the Study:
- To review the molecular basis of cardiac regeneration.
- To explore the role of noncoding RNAs, including microRNAs and long noncoding RNAs, in cardiomyocyte self-renewal and division.
- To identify key regulators for promoting cardiomyogenesis and advancing cardiac repair therapies.
Main Methods:
- Literature review of current evidence on cardiac regeneration.
- Analysis of molecular mechanisms involving microRNAs and long noncoding RNAs in cardiomyogenesis.
- Discussion of current limitations and future opportunities in harnessing these regulatory mechanisms.
Main Results:
- Noncoding RNAs, specifically microRNAs and long noncoding RNAs, are identified as critical regulators of cardiomyocyte division.
- Evidence suggests these noncoding RNAs play significant roles in the limited regenerative capacity observed in the mammalian heart.
- Elucidating their functions is a prerequisite for therapeutic development.
Conclusions:
- Noncoding RNAs are pivotal in controlling cardiomyocyte proliferation and cardiac regeneration.
- Targeting microRNAs and long noncoding RNAs offers potential therapeutic avenues for myocardial regeneration.
- Further research into these regulatory mechanisms is essential for advancing treatments for heart failure and cardiac injury.
Abstract:
The adult mammalian heart is incapable of regeneration following cardiac injury, leading to a decline in function and eventually heart failure. One of the most evident barriers limiting cardiac regeneration is the inability of cardiomyocytes to divide. It has recently become clear that the mammalian heart undergoes limited cardiomyocyte self-renewal throughout life and is even capable of modest regeneration early after birth. These exciting findings have awakened the goal to promote cardiomyogenesis of the human heart to repair cardiac injury or treat heart failure. We are still far from understanding why adult mammalian cardiomyocytes possess only a limited capacity to proliferate. Identifying the key regulators may help to progress towards such revolutionary therapy. Specific noncoding RNAs control cardiomyocyte division, including well explored microRNAs and more recently emerged long noncoding RNAs. Elucidating their function and molecular mechanisms during cardiomyogenesis is a prerequisite to advance towards therapeutic options for cardiac regeneration. In this review, we present an overview of the molecular basis of cardiac regeneration and describe current evidence implicating microRNAs and long noncoding RNAs in this process. Current limitations and future opportunities regarding how these regulatory mechanisms can be harnessed to study myocardial regeneration will be addressed.
