🧬 Senescence isn’t just about aging — it’s about how your cells respond to stress.

According to Moiseeva et al. (2022, The FEBS Journal), cellular senescence is a protective state triggered by DNA damage, oxidative stress, trauma, or metabolic strain. It’s part of the body’s natural defense system — a way to pause damaged cells from dividing.

But here’s the catch: when stress is chronic and unresolved, and the body can't adapt, senescence shifts from adaptive to maladaptive — and that’s where trouble begins.

📉 In the lens of Hans Selye’s General Adaptation Syndrome (GAS):

1. Alarm: Acute stress activates survival pathways.

2. Resistance: The body adapts and copes.

3. Exhaustion: Chronic stress overwhelms systems → maladaptation → senescence.

Senescent cells don’t just sit idle. They secrete a toxic brew called the SASP (Senescence-Associated Secretory Phenotype) — including inflammatory cytokines (like IL-6, TNF-α), growth factors, and matrix-degrading enzymes.

🔥 The result?

• Chronic inflammation

• Tissue breakdown

• Immune dysfunction

• And a key driver of diseases like:

  • Fibrosis

  • Neurodegeneration

  • Type 2 diabetes

  • Osteoarthritis

  • Cancer progression

🚫 Chronic senescence ≠ healthy aging.

It’s a sign of maladaptation — when the body's attempt to cope with stress goes too far, leading to lasting damage at the cellular level.

💡 The good news? We can intervene.

Targeting senescence and SASP is emerging as a promising strategy to slow, prevent, or even reverse age-related decline — through:

• Senolytics

• Anti-inflammatory therapies

• Lifestyle interventions

• Regenerative medicine

🧠 Your life history shapes your cellular future.

Unresolved trauma, stress, and wear-and-tear can leave molecular scars. But with awareness and the right tools, we can prevent the progression from stress to dysfunction.

Protect your resilience. Interrupt maladaptation. Support regeneration.

Citation:Moiseeva, V., Cisneros, A., Calls Cobos, A., Beña Tárrega, A., Santos Oñate, C., Perdiguero, E., Serrano, A. L., & Muñoz-Cánoves, P. (2022). Context‐dependent roles of cellular senescence in normal, aged, and disease states. The FEBS Journal, 290(5), 1161–1185. https://doi.org/10.1111/febs.16573

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