Cellular Senescence
The 'zombie' cells that neither die nor divide — and poison their surroundings
Definition
Cellular senescence is a state in which a cell permanently stops dividing but does not die. These 'zombie' or senescent cells accumulate irreparable DNA damage and respond by entering senescence rather than dying through apoptosis. The problem: they actively secrete an inflammatory cocktail called SASP (Senescence-Associated Secretory Phenotype) that damages neighbouring healthy cells, propagates senescence in surrounding tissue, and generates systemic inflammaging.
Detailed explanation
Cellular senescence is a cancer-protection mechanism: by halting the proliferation of cells with damaged DNA, it prevents them from becoming tumourigenic. The problem is that with ageing, millions of senescent cells accumulate that the immune system (particularly NK cells) can no longer efficiently clear.
The SASP includes IL-6, IL-8, TNF-α, MMPs (matrix metalloproteinases that degrade the extracellular matrix), growth factors, and chemokines. This chronic secretion produces local and systemic inflammation, tissue degeneration, and activation of further senescent cells.
Strategies for eliminating senescent cells (senolytics): quercetin + dasatinib (the most studied protocol in humans), fisetin, navitoclax, and ABT-263. Hyperbaric oxygen therapy at 2 ATA demonstrated in the Shamir study (2020) a 37% reduction in senescent CD28null T cells (an immune senescence marker) after 60 sessions.
In 2021, the first clinical trial using senolytics in humans (dasatinib + quercetin in idiopathic pulmonary fibrosis) showed significant functional improvement.
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