Macrophage Activities in Myocardial Infarction and Heart Failure

Abstract

Heart diseases remain the major cause of death worldwide. Advances in pharmacological and biomedical management have resulted in an increasing proportion of patients surviving acute heart failure (HF). However, many survivors of HF in the early stages end up increasing the disease to chronic HF (CHF). HF is an established frequent complication of myocardial infarction (MI), and numerous influences including persistent myocardial ischemia, shocked myocardium, ventricular remodeling, infarct size, and mechanical impairments, as well as hibernating myocardium trigger the development of left ventricular systolic dysfunction following MI. Macrophage population is active in inflammatory process, yet the clear understanding of the causative roles for these macrophage cells in HF development and progression is actually incomplete. Long ago, it was thought that macrophages are of importance in the heart after MI. Also, though inflammation is as a result of adverse HF in patients, but despite the fact that broad immunosuppression therapeutic target has been used in various clinical trials, no positive results have showed up, but rather, the focus on proinflammatory cytokines has proved more benefits in patients with HF. Therefore, in this review, we discuss the recent findings and new development about macrophage activations in HF, its role in the healthy heart, and some therapeutic targets for myocardial repair. We have a strong believe that there is a need to give maximum attention to cardiac resident macrophages due to the fact that they perform various tasks in wound healing, self-renewal of the heart, and tissue remodeling. Currently, it has been discovered that the study of macrophages goes far beyond its phagocytotic roles. If researchers in future confirm that macrophages play a vital role in the heart, they can be therapeutically targeted for cardiac healing.

Surface characteristics on commercial dental implants differentially activate macrophages in vitro and in vivo

“…One limitation of our in vivo study is that the implants were instrumented in soft tissue due to implant size instead of bone. We do not believe that macrophage activation and initial inflammatory response would be affected; however, it is possible that different tissue resident macrophages could be predetermine to activate to a more M2 phenotype as has been shown before (Burgess et al., 2019; SE et al., 2020).…”

Macrophages and the maintenance of homeostasis

“…Cardiac macrophages are now thought to participate in tissue remodeling and self-renewal of cardiac tissue. 65 As self-reactive T cells have been clonally deleted during development, the contribution of antigen-specific lymphocytes has been deemed to be minimal. Thus, the process of wound healing in the heart occurs in the absence of IL-4 and without the contribution of adaptive immunity.…”

PUFA Supplementation and Heart Failure: Effects on Fibrosis and Cardiac Remodeling

“…Both cardiac inflammation and fibrosis are being studied in numerous animal models, as they could be the target of new heart failure therapies [ 3 ]. Experimental and clinical studies conducted over the years in patients with acute and chronic heart failure have demonstrated the involvement of both the innate and adaptive immune systems in the disease [ 17 , 18 , 19 ]. In 2019, the CANTOS (Canakinumab Anti-Inflammatory Thrombosis Outcomes Study) trial, using anti-cytokine therapy with a monoclonal antibody against IL-1β, established that chronic inflammation plays an important role in the pathogenesis of heart failure.…”