Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacologyJul 16, 2026

Long-Term Infection and Heart Aging: New Insights into Infection-Linked Heart Muscle Disease

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Jul 17, 2026

Abstract

Chronic infections may act as significant catalysts for cardiac decline by inducing aging phenotypes.

Cardiovascular diseases are the leading cause of global mortality, with advanced age being the most significant risk factor.
Chronic infections can create a state of persistent inflammation, known as inflammaging, which resembles the inflammation associated with natural aging.
Infections can disrupt heart function by triggering cellular aging in heart cells through altered signaling pathways.
Chronic infections may lead to mitochondrial dysfunction and increased production of reactive oxygen species, causing oxidative damage in heart tissue.
The immune system's response to these infections may accelerate structural changes in the heart, including hypertrophy and fibrosis.

Simplified

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.

Funding

Competing interests

No competing financial interests reported.

PubMed

Long-Term Infection and Heart Aging: New Insights into Infection-Linked Heart Muscle Disease

Abstract

Funding

Competing interests

You found one interesting study. We’ll send the next 7.

What Lands in Your Inbox Each Week:

Recent issues from the longevity & aging brief

Abstract

Funding

Competing interests

Related papers

You found one interesting study. We’ll send the next 7.

What Lands in Your Inbox Each Week:

Recent issues from the longevity & aging brief