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| http://dx.doi.org/10.1084/jem.2013237805062015c | DOI Listing |
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Sirt1 overexpression inhibits chondrocyte ferroptosis via Ftl deacetylation to suppress the development of osteoarthritis.
J Bone Miner Metab
January 2025
Universiti Kebangsaan Malaysia Health Science, UKM, 43600, Bandar Baru Bangi, Selangor, Malaysia.
Introduction: Osteoarthritis (OA) is a chronic degenerative joint disorder characterized by an imbalance in chondrocyte metabolism. Ferroptosis has been implicated in the pathogenesis of OA. The role of Sirt1, a deacetylase, in mediating deacetylation during ferroptosis in OA chondrocytes remains underexplored.
View Article and Find Full Text PDFMolecular hydrogen reduces dermatitis-induced itch, diabetic itch and cholestatic itch by inhibiting spinal oxidative stress and synaptic plasticity via SIRT1-β-catenin pathway in mice.
Redox Biol
December 2024
Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin, 300052, China; Tianjin Research Institute of Anesthesiology, Tianjin, 300052, China. Electronic address:
Chronic itch which is primarily associated with dermatologic, systemic, or metabolic disorders is often refractory to most current antipruritic medications, thus highlighting the need for improved therapies. Oxidative damage is a novel determinant of spinal pruriceptive sensitization and synaptic plasticity. The resolution of oxidative insult by molecular hydrogen has been manifested.
View Article and Find Full Text PDFMechanism of Sirtuin1-Mediated Deacetylation of p65-Mediated Ferroptosis of Hippocampal Neurons in Cerebral Injury after Cardiopulmonary Resuscitation in Rats.
Neurochem Res
January 2025
Department of Radiology, the Second Affiliated Hospital of Kunming Medical University, No.374 Yunnan-Burma Road, Wuhua District, Kunming, Yunnan, 650101, PR China.
Objective: Post-resuscitation brain injury is a common sequela after cardiac arrest (CA). Increasing sirtuin1 (SIRT1) has been involved in neuroprotection in oxygen-glucose deprivation (OGD) neurons, and we investigated its mechanism in post-cardiopulmonary resuscitation (CPR) rat brain injury by mediating p65 deacetylation modification to mediate hippocampal neuronal ferroptosis.
Methods: Sprague-Dawley rat CA/CPR model was established and treated with Ad-SIRT1 and Ad-GFP adenovirus vectors, or Erastin.
Lithocholic acid binds TULP3 to activate sirtuins and AMPK to slow down ageing.
Nature
December 2024
State Key Laboratory for Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Lithocholic acid (LCA) is accumulated in mammals during calorie restriction and it can activate AMP-activated protein kinase (AMPK) to slow down ageing. However, the molecular details of how LCA activates AMPK and induces these biological effects are unclear. Here we show that LCA enhances the activity of sirtuins to deacetylate and subsequently inhibit vacuolar H-ATPase (v-ATPase), which leads to AMPK activation through the lysosomal glucose-sensing pathway.
View Article and Find Full Text PDFThe Role of Calorie Restriction in Modifying the Ageing Process through the Regulation of SIRT1 Expression.
Subcell Biochem
December 2024
Institute for Health and Sport, Victoria University, Melbourne, VIC, Australia.
Calorie restriction (CR), as a dietary approach of reducing caloric intake while maintaining nutritional adequacy, has gained significant attention due to its potential role in promoting longevity and enhancing health. Central to the beneficial effects of CR is SIRT1. SIRT1 belongs to a family of NAD+ dependent deacetylases and plays an important role in regulating various cellular processes, including histone deacetylation, oxidative stress response, and mitochondrial biogenesis.
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