What is the Origin of Molecular Senescence?

The concept originated in cell culture studies with the observation that cells stop dividing after a fixed number of passages, known as the Hayflick limit. The term has since been expanded in gerontology to encompass the detrimental systemic effects of these accumulating, metabolically deranged cells in the living organism.

What is the Mechanism of Molecular Senescence?

Senescence is typically triggered by persistent DNA damage or the activation of oncogenes, leading to the activation of powerful tumor suppressor pathways like p53 and p16. While initially a protective mechanism against cancer, the accumulation of senescent cells and their inflammatory SASP disrupts the local tissue microenvironment. This molecular disruption accelerates the aging of surrounding healthy cells and severely impairs the body's intrinsic tissue repair and regenerative mechanisms.

Molecular Senescence ∞ Area

Molecular Senescence

Meaning

Molecular Senescence is a state of irreversible growth arrest and profound altered function in individual cells, which is typically triggered by various forms of cellular stress, such as critically short telomeres or irreparable DNA damage. These non-dividing, metabolically active senescent cells accumulate with advancing age and secrete a complex mixture of pro-inflammatory molecules known as the Senescence-Associated Secretory Phenotype (SASP). This phenomenon is a fundamental, non-negotiable driver of chronic systemic inflammation, tissue dysfunction, and overall biological aging.