Senescence and SASP Are Potential Therapeutic Targets for Ischemic Stroke

Senescence Stroke
DOI: 10.3390/ph17030312 Publication Date: 2024-02-28T12:56:02Z
ABSTRACT
Aging is a known co-morbidity of ischemic stroke with its risk and severity increasing every year past 55+. While many the current therapies have shown success in reducing mortality, post-stroke morbidity has not seen same substantial reduction. Recently, involvement cellular senescence SASP brain injury neurological degeneration been recognized. Ischemic causes oxidative stress mitochondrial damage that induces through activation p21 p16 pathways, ultimately leading to synthesis release senescence-associated secretory phenotype (SASP). This event stress-induced premature (SIPS), aging decades beyond standard biological age due an increase senescent cells core ipsilateral hemisphere. Therefore, target SASP, including senolytics, senomorphic drugs, stem cell therapies, other cell-specific interventions, may be new path for treatment.
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