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Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart
Published on: June 14, 2020
Chronic Infection and Cardiac Aging: a New Perspective on Pathogen-Associated Cardiomyopathy
Noah Walsh1,2, Sophia DeCesare1, Kavisha Patel3
1Department of Biological Sciences, Binghamton University, Binghamton, NY, USA.
Insights
Chronic infections accelerate cardiovascular aging and disease by promoting inflammation and cellular damage. Targeting infections is key to enhancing heart health and longevity in older adults.
Area of Science:
- Cardiovascular Science
- Gerontology
- Immunology
Background:
- Cardiovascular diseases (CVDs) are a leading cause of death globally, with aging as a primary risk factor.
- Chronic infections are increasingly recognized as contributors to accelerated aging and cardiac dysfunction.
- Inflammaging, a chronic inflammatory state, is exacerbated by persistent infections, mimicking natural senescence.
Purpose of the Study:
- To investigate the role of chronic infections in premature cardiovascular aging.
- To elucidate the mechanisms by which infections induce cardiac senescence and dysfunction.
- To highlight anti-infective strategies for cardiovascular longevity.
Main Methods:
- Review of emerging evidence on infection-induced aging phenotypes in the heart.
- Analysis of molecular pathways including mTOR signaling, autophagy, and oxidative stress.
- Examination of structural cardiac changes associated with chronic infection and immune dysregulation.
Main Results:
- Chronic infections induce inflammaging, characterized by cytokine signaling and leukocyte infiltration.
- Infections trigger cardiomyocyte senescence via mTOR dysregulation and impaired autophagy.
- Mitochondrial dysfunction, ROS overproduction, and DNA damage contribute to myocardial exhaustion.
- Immune subversion accelerates cardiac remodeling, hypertrophy, and fibrosis.
Conclusions:
- Chronic infection is a modifiable driver of biological aging and cardiovascular disease.
- Anti-infective strategies are crucial for promoting cardiovascular longevity.
- Integrating anti-infective approaches into geriatric care is essential for heart health.
Abstract:
Cardiovascular diseases remain the primary driver of global mortality, with advanced age serving the most significant risk factor for their development and progression. Emerging evidence suggests that chronic infections can act as potent catalysts for cardiac decline by prematurely inducing aging phenotypes. Pathogens, including viruses, bacteria, and parasites, that evade host clearance establish a state of permanent inflammaging: a chronic, low-grade inflammatory milieu characterized by persistent cytokine signaling and leukocyte infiltration. This environment directly mirrors the sterile inflammation that drives natural senescence. Mechanistically, chronic infection subverts the heart's homeostatic pathways, triggering cardiomyocyte senescence through the dysregulation of mTOR signaling and the impairment of autophagy. These infections further drive mitochondrial dysfunction and the overproduction of reactive oxygen species (ROS), leading to oxidative DNA damage and metabolic exhaustion within the myocardium. On a structural level, immune subversion, via macrophage polarization and the induction of autoimmunity, accelerates left ventricular hypertrophy, myocardial remodeling, and interstitial fibrosis. By characterizing chronic infection as a modifiable driver of biological aging, we can prioritize anti-infective strategies as essential components of cardiovascular longevity and geriatric care.
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