Aging‑Cell Senescence Pathways: A Short Overview
Scientists study why cells stop dividing. This state is called senescence. It is a key factor in aging.
What triggers senescence?
DNA damage can activate the pathway. Telomere shortening also signals aging. Oxidative stress adds to the damage. Oncogene activation can force cells into senescence.
Main signaling routes
The p53‑p21 axis is central. DNA damage triggers p53. p53 raises p21 levels. p21 halts the cell cycle.
The Rb‑p16INK4a route is also vital. Stress signals increase p16INK4a. p16INK4a binds Rb. Rb keeps E2F transcription factors inactive.
Both routes converge on the cyclin‑dependent kinase inhibitors. They stop cell division.
Senescence‑associated secretory phenotype (SASP)
Senescent cells release many factors. These include cytokines, chemokines, and proteases. SASP can inflame nearby tissue. It can also alter the micro‑environment.
Impact on aging
Chronic SASP drives tissue dysfunction. It contributes to frailty and disease. Removing senescent cells can improve health in mice.
Therapeutic approaches
Senolytics aim to kill senescent cells. Dasatinib and quercetin are early examples. Senomorphics try to mute SASP.
Gene therapy is being tested. CRISPR tools target p16INK4a‑expressing cells.
Lifestyle factors can help. Caloric restriction lowers SASP levels. Exercise reduces systemic inflammation.
Future directions
Researchers map the full senescence network. They aim to find biomarkers for early detection. Combination therapies may prove more effective.
Aging‑cell senescence pathways link molecular stress to tissue decline. Understanding them may lead to longer, healthier lives.
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