(Re) Solving Repair After Myocardial Infarction

Abstract

Cardiovascular diseases, including myocardial infarction and its complications such as heart failure, are the leading cause of death worldwide. To date, basic and translational research becomes necessary to unravel the mechanisms of cardiac repair post-myocardial infarction. The local inflammatory tissue response after acute myocardial infarction determines the subsequent healing process. The diversity of leukocytes such as neutrophils, macrophages and lymphocytes contribute to the clearance of dead cells while activating reparative pathways necessary for myocardial healing. Cardiomyocyte death triggers wall thinning, ventricular dilatation, and fibrosis that can cause left ventricular dysfunction and heart failure. The ultimate goal of cardiac repair is to regenerate functionally viable myocardium after myocardial infarction to prevent cardiac death. Current therapies for heart failure after myocardial infarction are limited and non-curative. At the moment in clinic, conventional surgical interventions such as coronary artery bypass graft or percutaneous coronary interventions are only able to partially restore heart function, with a minor improvement in the left ventricular ejection fraction. The goal of this review is to provide an overview of endogenous myocardial repair mechanisms possibly transferable to future treatment strategies. Among the innovative factors identified as essential in cardiac healing, we highlight specialized pro-resolving mediators as the emerging factors that provide the key molecular signals for the activation of the reparative cells in the myocardium.

Cells of the Immune System in Cardiac Remodeling: Main Players in Resolution of Inflammation and Repair After Myocardial Infarction

“…The issue of targeted delivery of immune-modulating medications during MI also needs to be elaborated to avoid undesirable systemic effects. Current approaches propose to use hydrogels, patches, inhaled nano-particles, extracellular vesicles including exosomes and are reviewed in detail elsewhere ( 156 ). All the above mentioned techniques have certain dangers and drawbacks and require further studies of the bioavailability and safety in clinics.…”

Endophilin A2-mediated alleviation of endoplasmic reticulum stress-induced cardiac injury involves the suppression of ERO1α/IP3R signaling pathway

“…The decline in immediate mortality after MI has been well documented and is partially related to the use of more effective treatments, including angiotensin converting enzyme inhibitors, β-blockers, coronary revascularization, implantable cardioverter-defibrillators, and cardiac resynchronization therapeutic strategies [2,3]. However, a history of acute MI is associated with a 5-fold increase in the incidence of heart failure after 5 years of MI [4,5]. Therefore, great interest lies in the discovery of new therapeutic strategies to alleviate adverse cardiac injury and promote cardiac repair.…”

Novel Applications of Mesenchymal Stem Cell-Derived Exosomes for Myocardial Infarction Therapeutics

“…The current standard treatments for MI that aim to mitigate heart damage remain limited in restoring heart function as they fail to address the CMC and vasculature loss underlying the condition [5]. Major strides in several biomedical fields-especially that of stem cell biology and medicine-have appreciably attracted attention towards the research and development of cardiac regeneration strategies following MI [6][7][8].…”