Inflammaging: From Mechanisms to Clinical Implications and Targeted Interventions

May 1, 2026Aging and disease

Chronic Low-Level Inflammation in Aging: Causes, Health Effects, and Possible Treatments

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Longevity & Aging on OpenScience ↗PubMed ↗DOI ↗

Abstract

Inflammaging is associated with chronic, low-grade inflammation that may contribute to functional decline and multiple age-related diseases.

Elevated levels of damage-associated molecular patterns (DAMPs) and pro-inflammatory cytokines are linked to inflammaging.
Changes in immune cell composition and metabolic imbalance are characteristic of the inflammaging state.
The accumulation of senescent cells with a specific secretory phenotype may further exacerbate tissue vulnerability and functional decline.
Inflammaging is influenced by a combination of chronological aging, behavioral, environmental, psychosocial, and genetic factors.
Differentiating inflammaging from general chronic inflammation enhances understanding of its biological origins and clinical implications.

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Inflammaging refers to the chronic, low-grade, sterile inflammatory state that emerges as a hallmark of biological aging and is increasingly recognized as a contributor to functional decline, frailty, and the progression of multiple age-associated diseases. While acute inflammation supports host defense and tissue repair, persistent and unresolved inflammatory signaling promotes tissue damage, metabolic dysregulation, and impaired immune homeostasis. Inflammaging reflects a dysregulated physiological state associated with elevated damage-associated molecular patterns (DAMPs), pro-inflammatory cytokines, altered immune cell composition, metabolic imbalance, and the accumulation of senescent cells exhibiting a senescence-associated secretory phenotype (SASP). Together, these processes impair immune surveillance, increase oxidative stress, and tissue vulnerability, potentially accelerating functional decline and amplifying disease trajectories that may originate earlier in life. Despite ongoing challenges in precisely defining and measuring inflammaging, evidence suggests that its development is shaped not only by chronological aging but also by behavioral, environmental, psychosocial, and genetic factors, highlighting its dynamic and potentially modifiable nature. In this review, we distinguish inflammaging from general chronic inflammation, synthesize current understanding of its biological origins and mechanistic drivers, and examine its role in clinical outcomes including sarcopenia, neurodegeneration, and cardiovascular disease. We propose a conceptual translational framework linking biological mechanisms of inflammaging to multilayer biomarker signatures, AI-based risk stratification, and precision interventions. Additionally, we discuss the opportunities and limitations of these approaches for identifying individuals at risk for chronic disease and informing multi-dimensional strategies to promote resilience and extend health-span.

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Inflammaging: From Mechanisms to Clinical Implications and Targeted Interventions

Abstract

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