Ask about this productRelated genes to: HIBCH antibody
- Gene:
- HIBCH NIH gene
- Name:
- 3-hydroxyisobutyryl-CoA hydrolase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-07
- Date modifiied:
- 2016-10-05
Related products to: HIBCH antibody
Related articles to: HIBCH antibody
- Lactate produced during glycolysis plays a critical role in pulmonary arterial hypertension (PAH) by mediating protein lactylation and other molecular effects. Targeting lactylation-related signaling holds significant promise for the treatment of PAH. Therefore, we aimed to investigate lactylation-associated gene signatures and identify the critical role of hub genes. Transcriptomics analysis and mendelian randomization (MR) were applied to screen hub lactylation-related genes. 3-hydroxyisobutyryl-CoA hydrolase (HIBCH) was identified as a hub lactylation-related gene. HIBCH was significantly upregulated in platelet-derived growth factor (PDGF) stimulated pulmonary arterial smooth muscle cells (PASMCs) and lung tissues in PAH. MR analysis revealed that HIBCH upregulation correlated with higher PAH risk. Subsequently, the cell viability, proliferation and migration were detected to elucidate the effects of HIBCH on PASMCs. HIBCH knockdown markedly reduced the PDGF-induced lactate production, proliferation and migration in PASMCs. Further, cyproheptadine was screened as a potential HIBCH inhibitor. Cyproheptadine suppressed PASMCs proliferation and alleviated the monocrataline-induced pulmonary hypertension in vivo. Together, we identified the lactylation-related gene HIBCH as a risk factor for PAH and provided a novel therapeutic candidate for the treatment of PAH. - Source: PubMed
Publication date: 2026/03/05
Wu BojiTian TingtingLiu YuxiangQin ShixinMa XingyuZhang JihangLiu ChuanLiu XiLi JiuxuanQin Zhexue
- Source: PubMed
- Bioinformatic analysis of fatty acid metabolism-related genes (FAMRGs) in systemic sclerosis (SSc) patients' peripheral blood mononuclear cell (PBMC) expression profiles and clinical significance analysis provides SSc pathogenesis insights. - Source: PubMed
Publication date: 2026/01/02
Wang YangYu XiangLei TianyiLi XiuZhong LinruiWang ShuruiZhang QuanboQing Yufeng - Hypertension (HTN) is a mitochondrial and metabolic disease. However, cause-effect connections between mitochondrial dysfunction and HTN remains uncharted. we focused on mitochondria-related genes, identifying potential causal-genes-relevant blood pressure (BP) using mitochondria-related genome-wide Mendelian randomization (MR). Through the summary statistics from cis-expression quantitative trait loci (cis-eQTL) datasets (human blood and artery), mitochondrial transcription factor A (TFAM), and genome-wide association studies (GWAS) datasets of BP indices (systolic blood pressure [SBP], diastolic blood pressure [DBP], pulse pressure [PP], and mean arterial pressure [MAP]) and HTN. we conducted a MR analysis to explore the potential causal relationship between mitochondrial-related genes and the BP indices, HTN. Sensitivity analysis and Bayesian colocalization were employed to validate this causal relationship. In aorta, HIBCH expression was negatively associated with SBP; OCIAD1 expression was positively associated with MAP. In tibial artery, HIBCH expression was negatively associated with SBP; OCIAD1 expression was positively associated with SBP, PP, and MAP; SLC25A37 was positively associated with MAP. In blood, LACTB expression was negatively associated with SBP, PP, and MAP; OCIAD1 expression was negatively associated with SBP and PP; and MTX1 expression was negatively associated with MAP. HARS2 expression was positively associated with SBP and PP; RAB24 and PRELID1 expression was positively associated with DBP; and NME6 expression was positively associated with SBP and DBP. In conclusion, the regulation of blood pressure correlates with mitochondria-related genes (HIBCH, SLC25A37 and OCIAD1 in artery; LACTB, OCIAD1, MTX1, HARS2, RAB24, PRELID1 and NME6 in blood). This study provides scientific evidence for specifically regulating BP phenotypes. - Source: PubMed
Publication date: 2025/11/14
Zhang HongruiLi XiaoyangLiu YichenLiang ZhuoshuaiLi RuofeiGao WenhuiWang BoZhang YuchenTian YuyangHu XinmengJin HuizhenQiu ShuangLi YongGu YuluLiu SiyuLiu YunkaiCheng YiShi JikangLiu Yawen - The progression of type 2 diabetes (T2D) is driven by pancreatic β-cell dysfunction and loss, yet current therapies fail to address this core pathophysiology. - Source: PubMed
Publication date: 2025/10/08
Yi MingFeng XingrongGuan QiuyueLiu YinLiu YunqiangSu Zhiguang