Category: cell biology
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Urolithin A improves Alzheimer’s disease
Urolithin A (UA) enhances cGAS-STING activation, promoting cytosolic DNA clearance and modulating innate immune responses. This makes UA a potential therapeutic option for diseases involving cGAS-STING pathway activation or cytosolic DNA accumulation, with no reported adverse effects in animal models and limited human trials. Further research in relevant animal models…
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Salidroside promotes healthy longevity
The study investigates the impact of salidroside (SA) from Rhodiola rosea on lifespan and healthspan. SA binds to HSP90, reducing oxidation and extending lifespan. It inhibits HSP90’s ATPase activity, affecting protein interaction and gene expression. This reveals SA’s potential as an anti-aging drug and antioxidative agent, crucial for human health.
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Urolithin A modulates the cGAS-STING signaling pathway
Urolithin A (UA) enhances cGAS-STING activation, promoting cytosolic DNA clearance and modulating innate immune responses. This makes UA a potential therapeutic option for diseases involving cGAS-STING pathway activation or cytosolic DNA accumulation, with no reported adverse effects in animal models and limited human trials. Further research in relevant animal models…
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TIP60 in aging and neurodegeneration
TIP60, a histone acetyltransferase, regulates diverse pathways like autophagy, DNA repair, and neuronal functions, impacting aging and neurodegeneration. It holds promise as a therapeutic target for Alzheimer’s disease. Drosophila models provide insight into its neurobiological roles. Understanding TIP60’s functions may contribute to maintaining cellular homeostasis and counteracting aging and neurodegeneration.
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Genomic instability and aging
The mammalian DNA damage response involves various repair pathways to address diverse DNA lesions caused by damaging agents like UV and chemicals. Genomic instability plays a critical role in aging, contributing to age-related diseases. To combat this, interventions like physical exercise, dietary restriction, supplementation, and DNA repair stimulation can attenuate…
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Nicotinamide riboside rescues Rev1 deficiency
Rev1 deficiency causes metabolic shift and mitochondrial dysfunction in MEFs. NAD+ precursor nicotinamide riboside can manipulate these effects. Autophagy decreases in Rev1-/- MEFs but can be restored with NR supplementation. Abnormal mitochondrial morphology can be partially reversed with NR, which also protects mitochondrial cristae. Rev1 deficiency leads to metabolic dysregulation,…