Ask about this productRelated genes to: SIRT1 antibody
- Gene:
- SIRT1 NIH gene
- Name:
- sirtuin 1
- Previous symbol:
- -
- Synonyms:
- SIR2L1
- Chromosome:
- 10q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-20
- Date modifiied:
- 2016-10-05
Related products to: SIRT1 antibody
Related articles to: SIRT1 antibody
- Sepsis-associated acute kidney injury (SA-AKI) is a frequent and severe complication of sepsis and is closely associated with increased mortality. Mitochondrial dysfunction and impaired energy metabolism are important contributors to SA-AKI pathogenesis. Silent information regulator 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, regulates cellular metabolism, oxidative stress, and mitochondrial homeostasis. However, its role in septic renal mitochondrial dysfunction remains incompletely understood. In this study, an LPS-induced NRK-52E rat kidney epithelial cell injury model and a cecal ligation and puncture (CLP)-induced sepsis rat model were established. SIRT1-related signaling was pharmacologically modulated using the SIRT1 activator SRT1720 or the SIRT1 inhibitor EX-527. Cell viability, SIRT1 mRNA and protein abundance, mitochondrial ultrastructure, oxidative stress, mitochondrial membrane potential, ATP content, ATPase activity, and non-esterified fatty acid levels were assessed. LPS exposure reduced SIRT1 expression in NRK-52E cells and was accompanied by decreased cell viability, mitochondrial structural damage, oxidative stress, and impaired energy metabolism. SRT1720 attenuated these changes, whereas EX-527 aggravated them. Similarly, in CLP-induced septic rats, renal SIRT1 expression was decreased, together with renal injury and mitochondrial metabolic dysfunction. SRT1720 ameliorated renal pathological injury and mitochondrial-related abnormalities, whereas EX-527 worsened these changes. These findings suggest that SIRT1 activation attenuates SA-AKI, at least partly by maintaining renal mitochondrial energy homeostasis. - Source: PubMed
Publication date: 2026/09/10
Zhu RuiYang HairongLiu LiGao YuanyuanGao Xiaofang - - Source: PubMed
Publication date: 2026/09/09
- Mitochondrial dysfunction is an important cause of sarcopenia, and TWEAK/Fn14, as one of the major muscle wasting cytokines, its role in the development of sarcopenia by regulating mitochondrial biogenesis remains unclear. Expression of TWEAK in old and young mice was both detected. TWEAK was silenced in C2C12 myocytes using lentiviral vectors. Immunofluorescence, western blot, real-time polymerase chain reaction (RT-PCR), and ELISA were enrolled to analyze the effects of TWEAK on myotube size, mitochondrial content, mitochondrial ROS, and inflammatory factors. Additionally, aged mice received two injections of AAV9 vectors at 15 and 17 months of age. Upon reaching 18 months of age, the effects of TWEAK knockdown on grip strength, muscle mass, and gastrocnemius muscle indices were evaluated. TWEAK/Fn14 expression was significantly increased in old mice (p < 0.001). Compared with young controls, old mice exhibited a significant decrease in grip strength (p < 0.001) and a significant increase in lean mass (p < 0.05), whereas no significant difference was observed in fat content. In DEX-treated C2C12 myotubes, TWEAK knockdown significantly increased myotube diameter, enhanced ATP content and mitochondrial quantity, upregulated protein expression of SIRT1, PGC-1α, and p-AMPK, and inhibited mitochondrial ROS, Ca levels, p-p38 expression, and the secretion of inflammatory cytokines (TNF-α, IL-1β, IL-6, and iNOS). In aged mice, TWEAK knockdown did not significantly alter forelimb grip strength or lean mass, but significantly increased fat mass (p < 0.05). Mechanistically, TWEAK knockdown promoted AMPK signaling, inhibited p38 MAPK activation, enhanced mitochondrial biogenesis, and reduced serum levels of IL-1β, IL-6, and iNOS (p < 0.05), whereas serum TNF-α levels showed no significant difference. TWEAK knockdown attenuates age-related skeletal muscle mass loss and improves mitochondrial biogenesis in skeletal muscle, accompanied by modulated inflammatory factor release and altered AMPK-p38 MAPK signaling activity. However, no significant improvement in forelimb grip strength was observed in the in vivo experiment. These findings indicate that TWEAK suppression may represent a promising strategy for preserving muscle mass and metabolic homeostasis during aging, though its capacity to fully restore functional capacity requires further investigation. - Source: PubMed
Publication date: 2026/08/14
Maimaitiwusiman ZhuoyaXuekelati SaiyareWang AnyanAiriken NadilaXu YanbinGuo ShukeYang YiningWang Hongmei - To explore the molecular mechanisms underlying the protective effect of acupuncture on ovarian function in mice with cyclophosphamide-induced premature ovarian insufficiency (POI) via transcriptomic analysis. - Source: PubMed
Publication date: 2026/09/10
Luo YuYu MengFeng Shi-YuHuang Su-NingXie Hai-ChuanZhang BeiNing YanWu Jia-Man - Sirtuins represent a family of highly conserved enzymes, initially identified as Silent Information Regulator 2 (Sir2) in yeast, where they serve as fundamental determinants of longevity. Overexpression of Sir2 in yeast significantly extends lifespan, while its deletion leads to shortened longevity. In mammals, sirtuins (SIRT1-7) represent a conserved family of NAD-dependent deacylases with diverse catalytic activities. While most members primarily function as deacetylases, SIRT4 exhibits mono-ADP-ribosylation activity, and SIRT5 uniquely targets negatively charged acyl groups, including lysine succinylation, malonylation, and glutarylation. These enzymes act as critical intracellular sensors and regulators widely distributed across diverse tissues. By targeting a broad array of protein substrates, they regulate core biological processes-including genomic stability, metabolism, inflammation, and stress responses. As cardiovascular diseases (CVDs) remain the primary cause of global mortality, driven by complex pathologies such as chronic inflammation and metabolic dysregulation, the sirtuin network has emerged as an indispensable regulator of cardiovascular health. This review systematically elucidates the pivotal roles of sirtuins in cardiovascular homeostasis. We provide an in-depth, subcellular perspective on how nuclear, cytoplasmic, and mitochondrial sirtuins synergistically protect against cardiovascular remodeling, atherosclerosis (AS), and heart failure (HF). Particular emphasis is placed on the molecular mechanisms modulating macrophage polarization and the mitigation of vascular inflammation via the NF-κB signaling pathway. Furthermore, we assess the therapeutic promise of caloric restriction (CR) and pharmacological activators, incorporating recent human clinical evidence. We propose a framework matching sirtuin-based interventions to disease tempo, advocating isoform and compartment-specific strategies for acute and chronic CVDs. - Source: PubMed
Publication date: 2026/09/10
Gao MinLi LanlanLi LinWu HanyuWu YunkunFu Lei