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--- aging [2025/11/29 08:29] – [why do we age?] wh
+++ aging [2025/11/29 09:02] (current) – [why do we age?] wh
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     * testosterone decline results in muscle wasting
     * the PTGS2/PGE2/EP4 pathway is required to induce and maintain the senescent phenotype of primary human keratinocytes (NHEKs), and that increased cellular PGE2 levels are a potential determinant of the initial steps of the age-related oncogenic process in skin cells (([[https://www.aging-us.com/article/206149/text|2024: Prostaglandin E2 regulates senescence and post-senescence neoplastic escape in primary human keratinocytes]]))
+    * the protein, 15-PGDH - termed a gerozyme due to its increase in prevalence as the body ages - is a master regulator of aging
+      * is a major driver behind age-related loss of muscle strength in mice
+      *  has been implicated in the reduced regeneration of cartilage, bone, nerve and blood cells(([[https://www.science.org/doi/10.1126/science.adx6649|2025: Inhibition of 15-hydroxy prostaglandin dehydrogenase promotes cartilage regeneration]]))
+      * 15-PGDH degrades prostaglandin E2. Inhibiting 15-PGDH activity, or increasing levels of prostaglandin E2, supports the regeneration of damaged muscle, nerve, bone, colon, liver and blood cells
     * reduced High Mobility Group Box 1 (ReHMGB1), a reduced form of a key extracellular senescence-associated secretory phenotype (SASP) factor, plays a critical role in transmitting senescence from aging cells to distant tissues. Senescent cells are known to secrete pro-inflammatory factors and signaling molecules-collectively known as SASP-which induce paracrine senescence in surrounding cells. (([[https://www.metabolismjournal.com/article/S0026-0495(25)00128-3/fulltext]]))
   * a 2024 study (([[https://www.news-medical.net/news/20240718/Breakthrough-in-aging-research-Blocking-IL-11-extends-lifespan-and-improves-health-in-mice.aspx]])) showed that in aging mice, the expression of IL-11 was upregulated in various types of cells and tissues and that the deletion of either the gene coding for IL-11 or the IL-11 receptor's alpha 1 subunit protected the mice against metabolic decline, frailty, and multimorbidity as they aged.