Affiliations 

  • 1 Centre for Tissue Engineering and Regenerative Medicine (CTERM), Faculty of Medicine, Universiti Kebangsaan Malaysia, Jalan Yaacob Latiff, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia
  • 2 School of Dental Sciences, Universiti Sains Malaysia, Kampus Kesihatan Kubang Kerian, 16150 Kubang Kerian, Kelantan, Malaysia
  • 3 Department of Biomedical Engineering, Faculty of Engineering, Universiti Malaya, 50603 Kuala Lumpur, Malaysia
Heliyon, 2022 Nov;8(11):e11624.
PMID: 36425431 DOI: 10.1016/j.heliyon.2022.e11624

Abstract

Cardiac muscle cells have an innate capacity to perceive and react to mechanical strain via a mechanism known as mechanotransduction, whereby the cardiac muscle cells are intrinsically capable of sensing and responding to mechanical strain. This process occurs in the heart when mechanical inputs are converted to biochemical processes that result in myocardial structure and function changes. Mechanotransduction and its downstream effects work as compensatory mechanisms during early load adaptation. However, prolonged, and aberrant loading may cause maladaptive remodeling, resulting in altered physiological function, pathological cardiac hypertrophy, and heart failure. The rapid advancement of stem cell research has raised the hopes of both patients and clinicians. Mesenchymal progenitors have become one of the most intriguing possibilities for treating illnesses ranging from cartilage abnormalities to heart issues. Their immunomodulatory properties have also allowed for allogenic usage, besides expanding their potential for cardiomyocyte applications. In the present review, we highlighted mesenchymal stem cells (MSCs) in cardiovascular mechanotransduction, differentiation of cardiomyocytes and the use of MSCs in cardiovascular disease and tissue engineering.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.