Ask about this productRelated genes to: UCP2 antibody
- Gene:
- UCP2 NIH gene
- Name:
- uncoupling protein 2
- Previous symbol:
- BMIQ4
- Synonyms:
- SLC25A8
- Chromosome:
- 11q13
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-11
- Date modifiied:
- 2016-04-28
Related products to: UCP2 antibody
Related articles to: UCP2 antibody
- Hepatic encephalopathy (HE) is a severe clinical condition with limited therapeutic options. Silybin, a principal bioactive constituent of milk thistle, is a natural compound known for its protective effects against various liver diseases and neurodegenerative disorders. Silibinin meglumine (SM), the meglumine salt of silybin, is widely used in the management of hepatic disorders. However, the therapeutic potential and mechanistic basis of SM in HE remain incompletely elucidated. In this study, SM reduced serum ammonia levels and improved hepatic function markers, including alanine transaminase, aspartate transaminase, and total bilirubin (TBil), in thioacetamide (TAA)-induced HE mice. SM also attenuated inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin-6 (IL-6) in both plasma and brain tissue, reduced the oxidative stress marker malondialdehyde, and increased glutathione levels. Furthermore, molecular docking, cellular thermal shift assay (CETSA), drug affinity responsive target stability (DARTS) assay, and microscale thermophoresis (MST) assay collectively indicated that uncoupling protein 2 (UCP2) may serve as a direct molecular target of SM in mitigating HE. Notably, SM downregulated UCP2 expression in liver tissue and alleviated oxidative stress and mitochondrial dysfunction through modulation of the UCP2/PINK1/Drp1/mitofusin-2 (MFN2)/LC3B pathway. Additionally, co-administration of a UCP2 inhibitor partially attenuated the antioxidant effects of SM; however, no statistically significant reduction was observed in alanine aminotransferase (ALT) and aspartate aminotransferase (AST). In summary, this study demonstrates that SM-mediated targeting of UCP2 enhances hepatic mitochondrial function and suppresses excessive mitophagy, thereby ameliorating TBil in TAA-induced HE. These findings suggest that SM may represent a promising therapeutic strategy for TAA-induced HE. - Source: PubMed
Li YueChen HongChen XinyiZhou ZhangqiuWang JiemanZhang YuanyuanZhang ShengpengHe HongliangKou Junping - -Aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the central nervous system and is involved in the development of neural tissue as well as the regulation of its functions. Meanwhile, GABA has also been demonstrated to confer multiple physiological benefits, including alleviating stress and improving metabolic homeostasis. This study investigated GABA effects on proliferation, differentiation, and temperature stress protection of bovine skeletal muscle satellite cells (BSCs). - Source: PubMed
Publication date: 2026/04/14
Manzoor AbidNaseem SajidaFu ZhiqiRuan ChaohuiLiu XuYan ChunriChoi SeonghoLi Xiangzi - Abdominal aortic aneurysm (AAA) is a life-threatening cardiovascular disease with few effective treatments. Iron, an essential trace element, influences cellular functional states through multiple pathways and has been implicated in the pathogenesis and development of AAA. Previous studies have associated iron deficiency (ID) with the phenotypic switching of vascular smooth muscle cells by affecting mitochondrial and endoplasmic reticulum function. In this study, we demonstrate the protective role of appropriate iron supplementation in the progression of AAA. Our data further showed that iron supplementation increases the abundance of regulatory T cells (Tregs) both in the peripheral immune system and in aortic tissues, contributing to its protective effect. Moreover, iron supplementation inhibits the expression of mitochondrial uncoupling protein 2 (UCP2) in Tregs, which in turn suppresses the phosphorylation of dynamin-related protein 1 (Drp1), thereby modulating the dynamic balance between mitochondrial fusion and fission. Our findings suggest that iron supplementation may serve as a potential intervention to delay and ameliorate the progression of AAA. - Source: PubMed
Publication date: 2026/04/22
Liu HuagangChen YuanyangYang YunzhaoWang ZhenHu XiaopingWu Qi - Although the cellular role of uncoupling protein 2 (UCP2) in tumorigenesis has been reported in various solid tumor models, its role in leukemogenesis remains elusive. Herein, we demonstrated that UCP2 was highly expressed in AML and significantly associated with poor prognosis and chemoresistance, suggesting that UCP2 can be used as a potential biomarker in acute myeloid leukemia. Mechanistically, and silencing of UCP2 significantly impairs acute myeloid leukemia cell growth and survival, accompanied by the disruption of mitochondrial homeostasis. Interestingly, RNA-sequencing analysis and metabolic mass spectrometry revealed that silencing UCP2 resulted in accumulated branched-chain amino acids (BCAAs), which induced oxidative stress through the PI3K/AKT/mTOR signaling pathway. Additionally, the lack of BCAAs restored leukemic cell growth and survival and decreased mitochondrial ROS production induced by inhibiting UCP2. More importantly, supplementation of BCAA enhanced the anti-tumor activity of genipin, a selective inhibitor that targets UCP2, resulting in significantly reduced acute myeloid leukemia blasts, increased mouse survival, and magnified oxidative stress. Taken together, our study elucidates the rationale of targeting the UCP2-BCAA-PI3K/AKT/mTOR signaling axis in leukemogenesis and provides a novel strategy for leveraging the metabolic dependencies of leukemic cells. - Source: PubMed
Publication date: 2025/08/05
Innocent Agida OkohiShen YajieGao YixuanSun RuixinAximujiang KasimujiangXu ZizhenCheng JinkeMa Jiao - Chlorfenapyr (CHL) is a widely used insecticide whose expanding application raises concerns about cardiotoxicity following both acute poisoning and chronic environmental exposure. The mechanisms underlying its cardiac injury remain unclear. This study investigated the role of ferroptosis and mitochondrial dysfunction in CHL-induced cardiotoxicity. Using H9c2 cardiomyocytes and a Sprague-Dawley rat model, we assessed the effects of CHL and interventions with the ferroptosis inhibitor Ferrostatin-1 (Fer-1) or the mitochondrial antioxidant MitoTEMPO. In vitro, CHL decreased cell viability and triggered mitochondrial dysfunction, mitochondrial reactive oxygen species (mtROS) burst, and downregulation of uncoupling protein 2 (UCP2). These events culminated in ferroptosis, evidenced by lipid peroxidation, GPX4 downregulation, and ACSL4 upregulation, all rescued by Fer-1 or MitoTEMPO. In vivo, CHL exposure impaired cardiac systolic function, reducing ejection fraction (EF) and fractional shortening (FS), elevated serum troponin I, and caused histopathological damage, which were ameliorated by Fer-1 or MitoTEMPO. Our findings suggest that CHL cardiotoxicity is associated with the downregulation of cardiac UCP2 expression, compromised mitochondrial redox homeostasis, and the activation of mtROS-mediated ferroptotic pathways. UCP2 and mitochondrial redox homeostasis may therefore represent candidate targets for intervention. - Source: PubMed
Publication date: 2026/04/17
Zhang YiZhou XukaiJiang YatingChen YuluZhu XueqiCheng JiJiang ZhenluoLe YuanjieDu Liwen