Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated

Abstract

Myocardial infarction is the leading cause of death and disability worldwide, and the development of new treatments can help reduce the size of myocardial infarction and prevent adverse cardiovascular events. Cardiac repair after myocardial infarction can effectively remove necrotic tissue, induce neovascularization, and ultimately replace granulation tissue. Cardiac inflammation is the primary determinant of whether beneficial cardiac repair occurs after myocardial infarction. Immune cells mediate inflammatory responses and play a dual role in injury and protection during cardiac repair. After myocardial infarction, genetic ablation or blocking of anti-inflammatory pathways is often harmful. However, enhancing endogenous anti-inflammatory pathways or blocking endogenous pro-inflammatory pathways may improve cardiac repair after myocardial infarction. A deficiency of neutrophils or monocytes does not improve overall cardiac function after myocardial infarction but worsens it and aggravates cardiac fibrosis. Several factors are critical in regulating inflammatory genes and immune cells’ phenotypes, including DNA methylation, histone modifications, and non-coding RNAs. Therefore, strict control and timely suppression of the inflammatory response, finding a balance between inflammatory cells, preventing excessive tissue degradation, and avoiding infarct expansion can effectively reduce the occurrence of adverse cardiovascular events after myocardial infarction. This article reviews the involvement of neutrophils, monocytes, macrophages, and regulatory T cells in cardiac repair after myocardial infarction. After myocardial infarction, neutrophils are the first to be recruited to the damaged site to engulf necrotic cell debris and secrete chemokines that enhance monocyte recruitment. Monocytes then infiltrate the infarct site and differentiate into macrophages and they release proteases and cytokines that are harmful to surviving myocardial cells in the pre-infarct period. As time progresses, apoptotic neutrophils are cleared, the recruitment of anti-inflammatory monocyte subsets, the polarization of macrophages toward the repair phenotype, and infiltration of regulatory T cells, which secrete anti-inflammatory factors that stimulate angiogenesis and granulation tissue formation for cardiac repair. We also explored how epigenetic modifications regulate the phenotype of inflammatory genes and immune cells to promote cardiac repair after myocardial infarction. This paper also elucidates the roles of alarmin S100A8/A9, secreted frizzled-related protein 1, and podoplanin in the inflammatory response and cardiac repair after myocardial infarction.

Excretory/secretory products from Trichinella spiralis adult worms ameliorate myocardial infarction by inducing M2 macrophage polarization in a mouse model

“…The immune cells mediated in the sterile inflammatory responses play dual roles in injury and protection during cardiac hypoxia and repair [ 46 , 47 ]. It is critical to keep the balance of the pro- and anti-inflammatory pathways during the course of MI to reduce inflammation-caused heart tissue injury and promote the repair and remodeling of cardiovascular structure [ 17 ]. In this study, we attempted to use Ts -AES as an alternative treatment approach for MI based on their powerful immunomodulatory and regulatory functions identified before [ 48 ].…”

“…Macrophage is one of the most abundant cell types infiltrated in the infarcted heart [ 16 ] and plays an important role in the initiating inflammatory responses and the afterward healing process of MI. Upon occurrence of MI, many blood monocytes infiltrate into the ischemic heart tissue and differentiate into macrophages [ 17 ]. Activated macrophages can be classified into two main categories: classically activated macrophage (M1 type) and alternative activated type (M2) [ 18 , 19 ].…”

Oxygen‐Releasing Hydrogels for Tissue Regeneration

“…[208] Reduced blood supply from damage can increase cell death, complicating repair. [207] Treatments like oxygen therapy, drugs, or surgery may be necessary to improve blood supply and aid healing. [209,210] Oxygen-releasing hydrogels have gained attention as a promising biomaterial for myocardial repair, especially in cases of myocardial infarction where heart muscle damage leads to irreversible scar formation and compromised cardiac function.…”

“…[ 206 ] Angiogenesis creates new blood vessels for regeneration. [ 207 ] Finally, fibrosis replaces some tissue with scar tissue, affecting muscle function. [ 208 ] Reduced blood supply from damage can increase cell death, complicating repair.…”

“…[ 208 ] Reduced blood supply from damage can increase cell death, complicating repair. [ 207 ] Treatments like oxygen therapy, drugs, or surgery may be necessary to improve blood supply and aid healing. [ 209,210 ]…”