SIRT3 antibody - middle region (ARP32388_T100)
- Known as:
- SIRT3 (anti-) - middle region (ARP32388_T100)
- Catalog number:
- arp32388_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SIRT3 antibody - middle region (ARP32388_T100)
Related genes to: SIRT3 antibody - middle region (ARP32388_T100)
- Gene:
- SIRT3 NIH gene
- Name:
- sirtuin 3
- Previous symbol:
- -
- Synonyms:
- SIR2L3
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-20
- Date modifiied:
- 2014-11-18
Related products to: SIRT3 antibody - middle region (ARP32388_T100)
Related articles to: SIRT3 antibody - middle region (ARP32388_T100)
- Ischemic cardiomyopathy ranks as a principal cause of death and incapacity worldwide. Myocardial ischemia‑reperfusion injury (MIRI) caused by percutaneous coronary intervention is a major threat in the treatment of ischemic cardiomyopathy. Although lactylation (Kla) is extensively implicated in numerous pathological processes, its role and specific effects in MIRI remain unclear. Lactylation proteomics was used to identify proteins with different modifications during ischemia‑reperfusion injury. Co‑immunoprecipitation experiments were utilized to detect isocitrate dehydrogenase 2 (IDH2) lactylation levels. Immuno-fluorescence staining was applied to confirm intracellular lactylation levels. TUNEL, DHE and MitoSOX staining were used to measure oxidative damage in cells and tissues. An oxygen consumption rate experiment and the ATP assay were conducted to determine mitochondrial function. Western blots were utilized to detect changes in proteins related to mitochondrial functional homeostasis and downstream signal alterations. Excessive lactate accumulation was observed in MIRI model mice. This accumulation exacerbated the decline in cardiac function and the damage to cardiomyocytes in mice after MIRI. The lactylation of IDH2 in mitochondria was found to play a regulatory role in mitochondrial dysfunction and MIRI. Regarding the mechanism, it was verified that high IDH2 K275 lactylation caused a reduction in its enzymatic activity and decreased the production of α‑ketoglutarate in the tricarboxylic acid cycle. Consequently, the activation of the AMPK pathway was inhibited, and mitochondrial damage and functional impairment were aggravated. It was also found that SIRT3 regulated and prevented IDH2 lactylation. The results of the present study indicated that IDH2 lactylation, which is elevated due to lactate accumulation and negatively regulated by SIRT3, contributes to the exacerbation of MIRI by regulating the functional homeostasis of mitochondria. This discovery offers a new therapeutic concept and target for MIRI prevention. - Source: PubMed
Publication date: 2026/04/17
Wang ChangsenShen SimanChen SuyunLin JindaLi SimengChen JianningCai ShuyunYuan XiaodongYang ZiqiangDing KunXu LiZhang Liangqing - This study aims to inform clinical decision-making by identifying metabolism-related biomarkers involved in the progression of osteoarthritis (OA). Four OA cartilage-related microarray datasets were downloaded from the GEO database. A metabolism-related differentially co-expressed gene signature (MDCGS) associated with OA was then identified through an integrative computational approaches of Weighted Gene Co-expression Network Analysis (WGCNA) and Linear Models for Microarray Data (LIMMA) in combination with machine learning tools. The optimal gene expression and functions were additionally explored in vitro and in vivo. Molecular docking and molecular dynamics simulations (MDs) were conducted to explore the mode of binding with the drug and its role in OA. - Source: PubMed
Publication date: 2026/04/16
Zhang QianLi JunShan GuangchangHuang Dongfeng - Metabolic memory-the persistent risk of diabetic complications after early hyperglycemia-drives progressive renal injury in diabetic kidney disease (DKD) sustained oxidative stress, inflammation, and epigenetic reprogramming. We synthesize clinical and experimental evidence showing the nicotinamide adenine dinucleotide (NAD)-SIRT3 (sirtuin 3) axis as a central mechanistic hub linking mitochondrial dysfunction to epigenetic and inflammatory programs in DKD metabolic memory, while evaluating restoration strategies. Integrating data from preclinical, cellular, and human studies, we review SIRT3 biology, compartment-specific renal effects (proximal tubule, podocyte, endothelium), downstream targets, and NAD/SIRT3-modulating interventions. Key findings show consistently reduced renal SIRT3 expression and activity, driving mitochondrial hyperacetylation, impaired fatty-acid oxidation, persistent ROS, NLRP3/NF-κB-mediated inflammation, and profibrotic signaling. Preclinical NAD restoration or SIRT3 activation (e.g., NMN, NR, honokiol, metformin, SGLT2 inhibitors) ameliorates mitochondrial dysfunction, oxidative stress, fibrosis, and albuminuria; however, clinical evidence regarding renal endpoints and SIRT3 engagement biomarkers remains scarce. Translationally, selective kidney-targeted SIRT3 activators, integration with renoprotective therapies, and validated SIRT3 activity biomarkers are priorities to determine if targeting the NAD-SIRT3 axis can mitigate metabolic memory and slow DKD progression. - Source: PubMed
Publication date: 2026/04/16
Zhang YufeiWang YudianQiao YuhangLiu LihengZhao HailingJin QiPeng LiangLi Ping - Ferroptosis has recently been recognised as an immunogenic form of regulated cell death. Nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme in the NAD salvage pathway, is highly expressed in glioblastoma and represents a promising metabolic target. - Source: PubMed
Publication date: 2026/03/31
Zhao DongxuDuan LinRen HangZhang HangZhang MenghuiLiu ZhuohangWang HailanLu WenxuanShi WenhanHou QingwangLi TianxiaoLi Ming - Middle-aged/older (MA/O) men with low testosterone have greater oxidative stress-mediated vascular endothelial dysfunction, a major risk factor for cardiovascular disease (CVD). Testosterone deficiency impairs mitochondria, a source and target of oxidative stress. Whether the greater vascular endothelial dysfunction in MA/O men with low testosterone is related to mitochondrial dysfunction is unknown. This cross-sectional study measured mitochondrial respiration in peripheral blood mononuclear cells (PBMCs), and regulators of mitochondrial function (i.e., sirtuins [SIRTs]), and oxidant burden in vascular endothelial cells from (1) young adult men with normal testosterone (18-40 years; serum testosterone ≥ 13.9 nmol/L [400 ng/dL]; n = 23); (2) MA/O men with normal testosterone (50-75 years; serum testosterone ≥ 13.9 nmol/L [400 ng/dL]; n = 57), and (3) MA/O men with low testosterone (50-75 years; serum testosterone < 10.4 nmol/L [300 ng/dL]; n = 21). PBMCs from MA/O men with low testosterone had reduced carbohydrate (2.96 ± 0.65 vs. 6.85 ± 0.77 pmol/s·million cells; p = 0.001) and lipid-supported (4.10 ± 0.67 vs. 6.23 ± 0.69 pmol/s·million cells; p = 0.047) state 2 respiration compared to young men, and lower carbohydrate-supported uncoupled respiration than age-matched men with normal testosterone (17.77 ± 2.91 vs. 24.9 ± 1.93 pmol/s·million cells; p = 0.046). SIRT3 arterial (0.64 ± 0.04 vs. 0.99 ± 0.08 FU; p = 0.003) and venous (0.61 ± 0.03 vs. 0.92 ± 0.07 FU; p = 0.003) expression was lower in endothelial cells from MA/O men with low testosterone compared to age-matched men with normal testosterone. This study highlights the potential role of mitochondrial respiration and regulation in accelerated vascular aging in hypogonadal MA/O men. Importantly, these findings provide promising evidence for clinical therapeutic interventions to target mitochondrial health and SIRT3 to mitigate accelerated vascular aging in hypogonadal MA/O men. - Source: PubMed
Nguyen Branden LKehmeier Mackenzie NBabcock Matthew CDuBose Lyndsey EHildreth Kerry LStauffer Brian LRosenberry RyanKeller Amy CSteinke KiraMiles KalebGuerrero LucasKohrt Wendy MReusch JaneClayton Zachary SMoreau Kerrie L