Considering Cause and Effect of Immune Cell Aging on Cardiac Repair after Myocardial Infarction

The importance of the immune system for cardiac repair following myocardial infarction is undeniable; however, the complex nature of immune cell behavior has limited the ability to develop effective therapeutics. This limitation highlights the need for a better understanding of the function of each immune cell population during the inflammatory and resolution phases of cardiac repair. The development of reliable therapies is further complicated by aging, which is associated with a decline in cell and organ function and the onset of cardiovascular and immunological diseases. Aging of the immune system has important consequences on heart function as both chronic cardiac inflammation and an impaired immune response to cardiac injury are observed in older individuals. Several studies have suggested that rejuvenating the aged immune system may be a valid therapeutic candidate to prevent or treat heart disease. Here, we review the basic patterns of immune cell behavior after myocardial infarction and discuss the autonomous and nonautonomous manners of hematopoietic stem cell and immune cell aging. Lastly, we identify prospective therapies that may rejuvenate the aged immune system to improve heart function such as anti-inflammatory and senolytic therapies, bone marrow transplant, niche remodeling and regulation of immune cell differentiation.

Medienart:

E-Artikel

Erscheinungsjahr:

2020

Erschienen:

2020

Enthalten in:

Zur Gesamtaufnahme - volume:9

Enthalten in:

Cells - 9(2020), 8 vom: 13. Aug.

Sprache:

Englisch

Beteiligte Personen:

Tobin, Stephanie W [VerfasserIn]
Alibhai, Faisal J [VerfasserIn]
Weisel, Richard D [VerfasserIn]
Li, Ren-Ke [VerfasserIn]

Links:

Volltext

Themen:

Aging
Anti-Inflammatory Agents
Immune system
Inflammation
Journal Article
Myocardial infarction
Research Support, Non-U.S. Gov't
Review
Therapeutics

Anmerkungen:

Date Completed 19.03.2021

Date Revised 19.03.2021

published: Electronic

Citation Status MEDLINE

doi:

10.3390/cells9081894

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM313973059