Genetic Engineering Publications - GEG Tech top picks
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Revolutionary CAR T-cell therapy shows promise in reversing age-related metabolic dysfunction

Revolutionary CAR T-cell therapy shows promise in reversing age-related metabolic dysfunction | Genetic Engineering Publications - GEG Tech top picks | Scoop.it
study evaluates senolytic CAR T-cell therapy targeting uPAR-positive cells in aged mice, showing its effectiveness in mitigating age-related metabolic dysfunction and offering a potential long-lasting treatment for aging-associated conditions.
BigField GEG Tech's insight:

Cellular senescence is an irreversible cell cycle arrest induced in response to stress. Under stressful conditions, matrix remodeling enzymes and pro-inflammatory cytokines are produced, termed Senescence-Associated Secretory Phenotype (SASP). In young individuals with physiological conditions, such as tumor suppression and wound healing, SASP facilitates the recruitment of immune cells, which facilitate tissue restoration and the elimination of senescent cells. In the elderly, senescent cells accumulate due to reduced immune system function and increased tissue damage. To date, most senescent therapies include small-molecule drugs that require repeated administration and poorly target the affected area. A recent study in Nature Aging evaluates the efficacy of a senolytic therapy based on CAR-T cells. This therapy targets urokinase plasminogen activator receptor (uPAR)-positive cells, which accumulate during aging. In this study, senolytic cell therapies were shown to alleviate symptoms associated with physiological aging, including metabolic dysfunction.

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In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming

In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming | Genetic Engineering Publications - GEG Tech top picks | Scoop.it
Cellular reprogramming by transient expression of Yamanaka factors ameliorates age-associated
symptoms, prolongs lifespan in progeroid mice, and improves tissue homeostasis in
older mice.
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Here, the scientists report that partial reprogramming by short-term cyclic expression of Oct4, Sox2, Klf4, and c-Myc (OSKM) ameliorates cellular and physiological hallmarks of aging and prolongs lifespan in a mouse model of premature aging.

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