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Cytoplasmic chromatin fragment formation pathways in senescent cells are a potential therapeutic target for modulation of inflammation in aging, which contributes to age-associated diseases.

There is now sufficient and diverse evidence to support a cogent argument that DNA damage plays a causal role in aging.

Innate antiviral factors do not always perfectly distinguish between self and foreign, and potential adverse effects of antiviral defense mechanisms for the host have been discussed.

Single cells are believed to be incapable of complex forms of learning, but reconsideration of historical studies and more recent developments suggest that this orthodoxy must now be reconsidered.

This review considers the evolutionary processes and physiological mechanisms that maintain or end pregnancy in mammals to formulate general, testable theoretical models that provide insights into the biology of parturition.

Ensemble fluidity, observed as synaptic turnover and temporal drift in neuronal patterns, supports memory-updating and flexibility while maintaining memory stability.

Long under-appreciated, fibroblast biology is a key aspect of understanding how the immune system responds to tumors and may hold the key to improving immunotherapy in this tricky space.

Modulation of the aging process through cell signaling represents a recent and exciting area of study with the potential for development of therapeutics to extend human health.

A comprehensive literature review delineates the current knowledge of how systemic context, such as age and obesity, can impact CD8⁺ T cell function, anti-tumor immunity, and immunotherapy responsiveness.

Despite evidence that ACE2 is the receptor for SARS-CoV-2, its limited expression in the respiratory system challenges the uniqueness of this entry route and role in the multifaceted COVID-19.