Ask about this productRelated genes to: PDHA1 Blocking Peptide
- Gene:
- PDHA1 NIH gene
- Name:
- pyruvate dehydrogenase E1 alpha 1 subunit
- Previous symbol:
- PDHA
- Synonyms:
- -
- Chromosome:
- Xp22.12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2017-08-08
Related products to: PDHA1 Blocking Peptide
Related articles to: PDHA1 Blocking Peptide
- This study aimed to investigate the developmental patterns of breast muscle and leg muscle in embryonic Pekin ducks, and to screen potential genes regulating their independent development and growth differences. Muscle weight and histological characteristics were measured at eight embryonic stages (E11, E13, E15, E17, E19, E21, E23, E25; n = 10). Transcriptome analysis was performed on breast muscle at E11, E13, E17, and E21, and on leg muscle at E17 and E21. The results showed that breast muscle weight exhibited an S-shaped growth pattern, while leg muscle weight increased significantly in a linear or quadratic trend with increasing embryonic age (P < 0.0001). Histological features indicated that mature myofibers appeared in leg muscle at E19, but were not observed in breast muscle until E23. KEGG enrichment analysis of differentially expressed genes showed that pathways such as cytoskeleton in muscle cells and oxidative phosphorylation were involved in skeletal muscle development. Using bioinformatics analyses including WGCNA and Mfuzz clustering, we screened 5 potential genes regulating breast muscle development (including MYOD1), 12 potential genes associated with leg muscle development (including SDHA), and 11 potential genes mediating the developmental differences between breast and leg muscle (including PDHA1). Notably, from E21 to E25, leg muscle maintained rapid development whereas breast muscle development entered a plateau phase, and this difference may be driven by genes related to energy metabolism. This study systematically clarified the developmental patterns of breast muscle and leg muscle in embryonic Pekin ducks, providing a basis for further dissecting the molecular mechanisms underlying the spatiotemporal development of avian skeletal muscle. - Source: PubMed
Publication date: 2026/04/16
Huo ZhenZhou ZhengkuiHou Shuisheng - Acute myocardial infarction (AMI) is a leading cause of death worldwide, characterised by systemic inflammation and metabolic disorders. Tetrahydropalmatine (THP) and berberine (BBR) are major alkaloids derived from and , respectively, both of which have been shown to be cardioprotective; however, whether their mechanisms differ remains unclear. In this study, we systematically compared THP and BBR in treating AMI using integrated spatial metabolomics (AFADESI-MSI), untargeted metabolomics, lipidomics, and molecular biology. The results showed that both compounds improved cardiac function, reduced fibrosis, and suppressed inflammation. Multi-omics revealed that although both regulate glycerophospholipid metabolism, their pathway preferences and functional roles diverge: THP primarily affects linoleic acid and acetylcholine metabolism with a greater propensity to restore membrane structural integrity, whereas BBR targets ether phospholipids and sphingolipids with preferential anti-inflammatory lipid modulation. At the enzymatic level, both downregulated CHKα, PEMT, ChAT, and PDHA1. A key difference is that THP uniquely upregulated acetylcholinesterase (AChE) mRNA expression, an effect absent with BBR. Spatial metabolomics directly visualised that both compounds reverse the accumulation of pro-inflammatory lysophosphatidylcholines (LPCs) and restore structural phosphatidylcholines (PCs) in the infarct region, thereby re-establishing regional lipid homeostasis. To our knowledge, this is the first integrated multi-omics comparison to suggest shared and distinct mechanisms of THP and BBR in AMI. Notably, the differential regulation of AChE, as visualised by spatial omics, may serve as a molecular basis for understanding their distinct therapeutic features, although further validation at the protein and enzymatic activity levels is warranted. - Source: PubMed
Publication date: 2026/08/21
Zhang ZixuanLin YixuanGao FengZhang NaJiao JingyiYin HuoliLiang TianzhenCui HerongBai DongLei Haimin - Uncoupling protein 2 (UCP2) is expressed in various tissues throughout the body, but its expression in the spleen exceeds that of other organs. However, the precise function of UCP2 for spleen physiology is unclear. The spleen acts as a hub connecting the nervous system and immune system to cardiovascular and metabolic diseases. Here, we analyzed the impact of hypertension on the spleen and the role of UCP2 in this process. Experiments were performed with UCP2-knockout rats and their wild-type littermates. Hypertension was induced by administering the nitric oxide inhibitor L-NAME via tap water. Genetic depletion of UCP2 increased spleen size (splenomegaly) and strongly impaired the expression of genes coding for mitochondrial proteins. Among them, genes coding for proteins involved in oxidative metabolism, such as pyruvate dehydrogenase alpha 1, and the detoxification of reactive oxygen species were down-regulated. Collectively, these alterations in metabolism favor glycolysis and proliferation. Moreover, NOS3 was among the strongest down-regulated genes in UCP2 rats, and the inhibition of nitric oxide synthase by L-NAME mimicked large parts of the expression profile. Neither the depletion of UCP2 nor L-NAME-induced hypertension or combinations thereof affected chronic inflammation. In summary, UCP2 controls fuel consumption in splenic cells in a nitric-oxide-dependent way. - Source: PubMed
Publication date: 2026/07/30
Wagner LeaSchreckenberg RolfItani NadjaSato TsuneshiroSperhake JuliaCesar YvaSchlüter Klaus-Dieter - Polycystic ovary syndrome (PCOS) is associated with metabolic disturbances within the follicular microenvironment that may impair oocyte competence. Although elevated acetate levels have been reported in the follicular fluid (FF) of PCOS patients, its metabolic fate and transcriptional impact in cumulus cells (CCs) remain unclear. This study investigated acetate-related metabolic reprogramming in CCs of women with PCOS. - Source: PubMed
Publication date: 2026/08/08
Safaeinejad ZahraValipour Motlagh AliRazavi FatemehEsmaeili MaryamRezvanian ParsaGhaedi-Heydari RasoolGhaderi Khorasgani AtefehDastjerdi SamaNasr-Esfahani Mohammad Hossein - While recent studies have established links between metabolic reprogramming and inflammatory senescence, the specific metabolic drivers in vascular aging remain incompletely defined. Here, we systematically characterized senescent phenotypes and targeted metabolomic profiles in primary aging endothelial cells, identifying a pyruvate dehydrogenase E1 component subunit alpha (PDHA1)-dependent metabolic shift as a hallmark of cellular senescence. Using a D-galactose-induced senescence model, we demonstrated that endothelial-specific knockdown alleviated pulmonary vascular endothelial senescence and associated functional decline. Further investigation revealed that PDHA1 hyperactivation disrupts mitochondrial homeostasis, leading to excessive mitochondrial reactive oxygen species production, oxidative mitochondrial DNA damage, and subsequent cytosolic mitochondrial DNA release, thereby triggering cyclic GMP-AMP synthase-mediated senescence. Mechanistically, decreased lactylation of PDHA1 at lysine 336 potentiated its activity and promoted dephosphorylation at serine 293. This posttranslational cross talk enhanced PDHA1 activation and drove a prosenescent metabolic shift. Together, our results elucidate that a previously unrecognized PDHA1 hyperactivation promotes endothelial senescence. - Source: PubMed
Publication date: 2026/08/20
Zhong Wen-JingYang Nan-Shi-YuZhang Chen-YuLiu Yu-BiaoJin LingOu An-JunChen HuiLi JuanZhou YongHe Bai-MeiDuan Jia-Xi