SIRT7 antibody
- Known as:
- SIRT7 (anti-)
- Catalog number:
- orb100696
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- SIRT7 antibody
Related genes to: SIRT7 antibody
- Gene:
- SIRT7 NIH gene
- Name:
- sirtuin 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-20
- Date modifiied:
- 2014-11-19
Related products to: SIRT7 antibody
Related articles to: SIRT7 antibody
- Myocardial ischemia-reperfusion injury (MIRI) is an inevitable pathological complication following reperfusion therapy for acute myocardial infarction. Massive reactive oxygen species burst, mitochondrial dysfunction, inflammatory cascade activation and multiple programmed cell death jointly aggravate irreversible cardiomyocyte loss, expanding infarct size and increasing the risk of progressive heart failure. As conserved NAD⁺-dependent deacetylases, the seven-member sirtuin (SIRT1-SIRT7) family exert widespread cardioprotective effects against MIRI, yet the subtype-specific molecular mechanisms, coordinated regulatory networks and translational bottlenecks lack systematic collation in existing reviews. This review aims to systematically summarize the regulatory pathways of all SIRT isoforms governing oxidative stress, mitochondrial homeostasis, inflammatory response and programmed cell death under MIRI, compare divergent biological functions among subtypes, sort out available SIRT-targeted pharmacological intervention strategies, and further clarify major obstacles restricting clinical translation, as well as prospective therapeutic targets for subsequent research. Distinguished by subcellular localization, nuclear, cytoplasmic and mitochondrial SIRT members participate in multi-layered myocardial defense. Nuclear SIRT1 coordinates AMPK-FOXO3-Nrf2 signaling to upregulate antioxidant enzymes and maintain mitophagic balance; mitochondrial SIRT3 dominates PINK1/Parkin-dependent mitophagy and deacetylates SOD2 to eliminate mitochondrial reactive oxygen species; cytoplasmic SIRT2 alleviates endoplasmic reticulum stress and restrains NLRP3 inflammasome activation; mitochondrial SIRT4 and SIRT5 stabilize mitochondrial fusion dynamics and eliminate lipid peroxidation via lysine desuccinylation, respectively; nuclear SIRT6 and SIRT7 relieve reperfusion inflammation, repair oxidative DNA damage and block late myocardial fibrosis. Collectively, the whole SIRT family forms an integrated endogenous protective network targeting all core pathological links of MIRI. In conclusion, SIRT1, SIRT3 and SIRT6 act as core cardioprotective subtypes: they synergistically activate the AMPK/Nrf2 antioxidant axis to block reperfusion oxidative injury. SIRT2, SIRT4, SIRT5 and SIRT7 serve auxiliary regulatory roles by balancing cardiac energy metabolism and maintaining genomic integrity. Current SIRT small-molecule agonists face prominent translational limitations including low oral bioavailability and poor myocardial tissue selectivity. Mitochondria or cardiomyocyte-targeted nano-delivery systems provide a feasible strategy to overcome such defects. Large animal MIRI models and prospective human clinical trials are urgently required to validate the long-term safety and therapeutic efficacy of SIRT-targeted interventions before clinical transformation. - Source: PubMed
Publication date: 2026/08/12
Xue TingtingWang ShuZhu XinyuLuo JialiZhu RuixiangLi HuihuiJu RuotongZhang PuhuaCui XiangrongJing Xuan - Glycosylphosphatidylinositol-specific phospholipase D1 (Gpld1) is a membrane-associated enzyme that modulates diverse cellular processes through the cleavage of glycosylphosphatidylinositol (GPI)-anchored proteins. Although recent studies have linked circulating Gpld1 to exercise-induced rejuvenation, its cell-autonomous role in coordinating redox homeostasis, melanogenesis, and cellular aging has not been fully elucidated. - Source: PubMed
Publication date: 2026/08/11
Lee Si EonKim Moon-Moo - Vitiligo is a common acquired depigmentation disorder affecting approximately 0.5-2% of the global population, characterized by the selective destruction of melanocytes leading to white patches on the skin. The pathogenesis of vitiligo involves complex interactions between genetic susceptibility, autoimmune responses, oxidative stress, and melanocyte dysfunction. Recent studies have demonstrated that ferroptosis, a novel iron-dependent form of programmed cell death, may play a critical role in melanocyte loss in vitiligo. Ferroptosis is characterized by iron accumulation, lipid peroxidation, glutathione (GSH) depletion, and decreased glutathione peroxidase 4 (GPX4) activity. This form of cell death differs fundamentally from apoptosis, necrosis, and autophagy in its morphological, biochemical, and genetic characteristics. Understanding the role of ferroptosis in vitiligo pathogenesis opens new avenues for therapeutic intervention and may explain why melanocytes in vitiligo patients are particularly vulnerable to oxidative damage. Multiple experimental and clinical studies have now confirmed the upregulation of ferroptosis biomarkers including transferrin receptor 1 (TFR1), malondialdehyde (MDA), and 4-hydroxynonenal (4-HNE) in vitiligo lesions, alongside downregulation of GPX4 and the cystine/glutamate antiporter System Xc-. Emerging evidence further implicates epigenetic regulators such as SIRT7 and RNA-binding proteins such as SLC3A2 in modulating melanocyte ferroptosis susceptibility. This comprehensive review systematically summarizes current knowledge on ferroptosis mechanisms in vitiligo, including the System Xc-/GPX4 axis, iron metabolism dysregulation, lipid peroxidation pathways, and their interactions with autoimmune responses. We also explore emerging therapeutic strategies targeting ferroptosis-related pathways, including iron chelation, GPX4 enhancement, lipid peroxidation inhibitors, NRF2 activators, and natural compounds such as baicalein. By integrating basic research findings with clinical observations, this review provides novel insights into vitiligo pathogenesis and establishes a theoretical foundation for developing innovative treatment strategies based on ferroptosis regulation. Crucially, by contrasting the ferroptosis-hypersensitive profile of vitiligo melanocytes with the ferroptosis-resistant molecular landscape of melanoma cells, this review proposes a novel framework for melanocyte-lineage-selective ferroptosis modulation as a therapeutic strategy. - Source: PubMed
Publication date: 2026/08/07
Zhang ChunyanXu Faming - Sirtuins (SIRT1-SIRT7) are a family of NAD+-dependent lysine deacetylases that possess mono-ADP-ribosyltransferase activity and integrate cellular metabolic status with chromatin regulation, genome maintenance, redox homeostasis, immune responses, and adaptation to cancer therapies. Their translational value has been obscured by a recurring paradox: the same isoform may constrain malignant transformation in one setting yet support metastatic competence, stemness, immune evasion, or drug resistance in another. This review reframes that paradox as a measurable problem of context. We define a SIRT context code in which NAD+ availability and compartmentalization, subcellular localization, PTM state, chromatin occupancy, oncogenic genotype, cell lineage, and tumor microenvironment jointly determine sirtuin output. Using recent mechanistic and translational evidence, we summarize how sirtuins regulate metabolic switching, histone acetylation and lactylation, genome stability, cancer-associated fibroblast programs, regulatory T-cell enrichment, cancer stem-cell plasticity, angiogenesis, and resistance to DNA-damaging, targeted, and immune therapies. We further argue that successful sirtuin pharmacology will require context matching rather than indiscriminate activation or inhibition. Priorities include spatial and single-cell biomarker discovery, compartment-specific NAD+ measurements, PTM-resolved activity assays, structure-guided isoform-selective agents, and degrader strategies targeting non-catalytic scaffolding functions. Sirtuins should therefore be viewed as metabolic-epigenetic decision nodes rather than fixed oncogenes or tumor suppressors. However, the evidence remains predominantly preclinical, and our search identified no clinical-stage oncology trials of direct sirtuin modulators using prospective biomarker stratification, underscoring that this framework remains translationally aspirational rather than clinically validated. - Source: PubMed
Publication date: 2026/08/02
Aly AbdelwahabTan ZhiqingSasidharan SreenivasanOon Chern Ein - Alopecia areata (AA) is an autoimmune disorder characterized by oxidative stress-induced dysfunction of hair follicle stem cells (HFSCs). Nicotinamide mononucleotide (NMN), a precursor of NAD, exhibits antioxidant properties, but its role and mechanism in AA remain unclear. This study aimed to investigate the therapeutic potential of NMN and its underlying mechanism. Scalp tissues from AA patients and healthy controls were collected, and HFSCs were isolated. An in vitro oxidative stress model was established using HO. Cell viability, apoptosis, migration, oxidative stress and glutamine metabolism were assessed. Molecular mechanisms were investigated via gene knockdown (sh-SIRT7, sh-GLS1) and rescue experiments with an acetylation-resistant GLS1 mutant (GLS1-MUT). An in vivo mouse model of HO-induced hair follicle damage was utilized for validation. The results showed that NMN (2 mM) significantly enhanced the viability, migration, and differentiation capacity of both AA-derived and HO-induced HFSCs, while cell apoptosis and oxidative stress were repressed. NMN also promoted glutamine metabolism with increased GSH, glutamate, glutamine and NAD levels, as well as elevated GPx and GLS1 activities. Mechanistically, SIRT7 expression was downregulated in AA. NMN restored SIRT7 expression and activity, leading to the deacetylation and activation of GLS1. Knockdown of SIRT7 or GLS1 abolished NMN's protective effects, which were rescued by GLS1-MUT, establishing a linear pathway. In vivo, NMN treatment alleviated HO-induced hair follicle damage, promoted regeneration, and preserved SIRT7 expression in the stem cell niche. In conclusion, NMN alleviates oxidative stress and improves HFSC function in AA by activating the SIRT7-GLS1 axis and enhancing glutamine metabolism, revealing a novel therapeutic target for AA. - Source: PubMed
Publication date: 2026/07/27
Cao TianyuJiang LanLiu LinWang NaZhai DaLiu Ling