AI Article Synopsis
- Myocardial infarction leads to the formation of scar tissue that disrupts heart function and can cause dangerous heart rhythm issues.
- The healing process involves various changes including inflammation, biochemical signaling, and alterations in cell activity and structure, all of which affect electrical conduction in the heart.
- Research into regenerating heart tissue hasn't yet provided significant improvements for heart disease treatment, but new therapeutic strategies focusing on modifying scar tissue show potential for enhancing heart function after a heart attack.
Article Abstract
Myocardial infarction results in scar tissue that cannot actively contribute to heart mechanical function and frequently causes lethal arrhythmias. The healing response after infarction involves inflammation, biochemical signaling, changes in cellular phenotype, activity, and organization, and alterations in electrical conduction due to variations in cell and tissue geometry and alterations in protein expression, organization, and function - particularly in membrane channels. The intensive research focus on regeneration of myocardial tissues has, as of yet, only met with modest success, with no near-term prospect of improving standard-of-care for patients with heart disease. An alternative concept for novel therapeutic approach is the rejuvenation of cardiac electrical and mechanical properties through the modification of scar tissue. Several peptide therapeutics, locally applied genetic therapies, or delivery of genetically modified cells have shown promise in improving the characteristics of the fibrous scar and post-myocardial infarction prognosis in experimental models. This review highlights several factors that contribute to arrhythmogenesis in scar formation and how these might be targeted to regenerate some of the electrical and mechanical function of the post-MI scar.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5113035 | PMC |
| http://dx.doi.org/10.1016/j.semcdb.2016.05.020 | DOI Listing |
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