Inflammation is a fundamental biological process that has evolved as an ancient defense mechanism responding to infection and injury, but its manifestation during aging varies widely depending on biological and environmental factors.

The concept of inflamm-aging is rooted in evolutionary biology, highlighting inflammation's role in responding to both infectious and sterile conditions like obesity, and its impact on aging-related decline.

There is no single biomarker for inflamm-aging; instead, studies rely on a variety of inflammatory mediators and signaling markers, reflecting its complex and context-dependent nature.

Inflamm-aging is linked to age-related cognitive and physical decline, with elevated inflammatory markers such as CRP, IL-6, and TNF-α commonly observed in older, especially frail, individuals.

Individual environmental and lifestyle histories, or exposomes, influence inflamm-aging trajectories, with factors like infections and diet affecting immune cell behavior and inflammation levels.

Inflammation involves intricate signaling networks, including cytokines with overlapping functions, organized in a 'bow-tie' structure that maintains a balance between robustness and efficiency.

Chronic, low-grade systemic inflammation, characteristic of inflamm-aging, involves immune system remodeling and the accumulation of senescent cells that produce pro-inflammatory mediators.

Viewing inflamm-aging as a reaction norm shaped by evolutionary mismatch emphasizes its complex, context-dependent nature and the difficulty in defining universal measures.

Inflamm-aging is observed across multiple species, supporting its fundamental role in aging, although some recent research suggests it may not be present in all populations, particularly some indigenous, non-industrialized groups.

The evolutionary origins of inflammation and cytokine signaling pathways are linked to cellular stress responses and environmental adaptation, which vary across species and ecological niches.

Historical shifts in human subsistence and environmental exposures have created evolutionary mismatches that influence inflamm-aging, affecting tissue health and disease susceptibility.