CD47 blockade reduces doxorubicin-induced cardiac aging in male mice
Inhibiting CD47 lessens heart dysfunction and blunts cellular senescence caused by the chemotherapy drug doxorubicin.
8 results
Inhibiting CD47 lessens heart dysfunction and blunts cellular senescence caused by the chemotherapy drug doxorubicin.
Conditioned medium from damaged astrocytes alters extracellular mitochondria and triggers ATP depletion and oxidative stress in human postmitotic neurons.
A screen of 800 natural compounds identified a phytochemical that activates autophagy and restores cell-cycle activity in models of cellular exhaustion.
Physical activity preserved cardiac function and sustained FNDC5 and irisin signaling in mice exposed to doxorubicin.
The formulation co-delivers rapamycin and doxorubicin across the mucus barrier to inhibit mTOR and suppress tumor growth without evident systemic toxicity.
Researchers found that senescent epithelial cells secrete TGF-beta1 to reprogram fibroblasts into a matrix-remodeling state, which senolytic treatment can blunt.