Acta biochimica et biophysica Sinica最新文献

lncRNA CHROMR promotes DLBCL viability and invasion in an m ⁶A-dependent manner. lncRNA CHROMR以m6a依赖的方式促进DLBCL的生存和侵袭。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-10-16 DOI: 10.3724/abbs.2026151

Chang Liu, Meina Wu, Chan Zhang, Yuejing Zhao, Yurun Du, Jiahui Hou, Ruihan Gao, Kun Yang, Feng Li, Tao Guan, Hongwei Zhang, Baofeng Yu

{"title":"lncRNA CHROMR promotes DLBCL viability and invasion in an m 6A-dependent manner.","authors":"Chang Liu, Meina Wu, Chan Zhang, Yuejing Zhao, Yurun Du, Jiahui Hou, Ruihan Gao, Kun Yang, Feng Li, Tao Guan, Hongwei Zhang, Baofeng Yu","doi":"10.3724/abbs.2026151","DOIUrl":"https://doi.org/10.3724/abbs.2026151","url":null,"abstract":"Long noncoding RNA (lncRNA) CHROMR is closely associated with the development of diffuse large B-cell lymphoma (DLBCL) and drug resistance to rituximab. However, the mechanism underlying the upregulation of the lncRNA CHROMR in DLBCL cells remains unknown. N 6-methyladenosine (m 6A) modifications are involved in the tumorigenesis and progression of numerous human cancers. This study reveals that m 6A complexes are enriched on the lncRNA CHROMR in DLBCL cells, as determined by methylated RNA immunoprecipitation-quantitative polymerase chain reaction (MeRIP-qPCR) assay and bioinformatics analysis. Our results demonstrate that methyltransferase-like 3 (METTL3) acts as the m 6A methylation writer for the lncRNA CHROMR at site 3 (\"UGGAACUU\"), while insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) functions as the reader of this modification. Together, they enhance the stability of the lncRNA CHROMR. Furthermore, both METTL3 and IGF2BP1 play critical roles in regulating the viability and invasion of DLBCL cells. These findings highlight the indispensable role of m 6A modification in the lncRNA CHROMR, revealing METTL3 and IGF2BP1 as epigenetic mediators that regulate CHROMR expression.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hepatocyte IER2 attenuates APAP-induced liver injury by regulating ACOT2-mediated lipid metabolism in mice. 肝细胞IER2通过调节acot2介导的脂质代谢减轻apap诱导的小鼠肝损伤。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-10-14 DOI: 10.3724/abbs.2026154

Peng Jiang, Lin Jiang, Linala Tuerxunjiang, Zhihua Wang, Zhenghong Liu, Meiming Su, Zhidan Zhang, Qian Wang, Shuxin Han, Jianping Weng, Suowen Xu

{"title":"Hepatocyte IER2 attenuates APAP-induced liver injury by regulating ACOT2-mediated lipid metabolism in mice.","authors":"Peng Jiang, Lin Jiang, Linala Tuerxunjiang, Zhihua Wang, Zhenghong Liu, Meiming Su, Zhidan Zhang, Qian Wang, Shuxin Han, Jianping Weng, Suowen Xu","doi":"10.3724/abbs.2026154","DOIUrl":"https://doi.org/10.3724/abbs.2026154","url":null,"abstract":"Acetaminophen (APAP)-induced liver injury (AILI) is a common serious adverse drug event, yet its molecular mechanisms remain incompletely understood. To identify key regulators in AILI, we conduct a temporal liver transcriptomic sequencing analysis in mice subjected to APAP exposure, revealing a significant and dynamic alteration in the expression of immediate early response 2 ( Ier2). Single-cell RNA sequencing analysis further delineates Ier2 expression patterns across hepatic cell populations following APAP insult. Hepatocyte-specific Ier2 knockout (HKO) mice and hepatocyte-directed Ier2 overexpression mice are generated to elucidate the molecular function of IER2 in AILI. RNA sequencing and proteomics are performed to investigate the underlying protective mechanisms of IER2 in AILI. We demonstrate that hepatocyte-specific Ier2 deletion increases susceptibility to AILI, whereas hepatic Ier2 overexpression ameliorates APAP-induced liver injury. Integrated transcriptomic and proteomic analyses identify lipid metabolism as a key pathway modulated by IER2 overexpression, with ACOT2 as a putative target. Functional rescue experiments reveal that ACOT2 knockdown markedly attenuates the protective effect of IER2, indicating that ACOT2 is required for IER2-mediated hepatoprotection. In conclusion, IER2 protects against AILI by modulating lipid metabolism pathways, with ACOT2 as a critical downstream effector. These findings position IER2 as a promising and novel therapeutic target for mitigating AILI.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Structural basis for phosphorylation-induced inactivation of the rice ammonium transporter AMT1;1. 磷酸化诱导水稻铵转运体AMT1失活的结构基础；

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-10-14 DOI: 10.3724/abbs.2026188

Fang Yu, Xiaowei Huang, Shuang Wang, Ning An, Peng Zhang, Jirong Huang, Xue Zhang

{"title":"Structural basis for phosphorylation-induced inactivation of the rice ammonium transporter AMT1;1.","authors":"Fang Yu, Xiaowei Huang, Shuang Wang, Ning An, Peng Zhang, Jirong Huang, Xue Zhang","doi":"10.3724/abbs.2026188","DOIUrl":"https://doi.org/10.3724/abbs.2026188","url":null,"abstract":"Ammonium (NH 4 +) uptake and transport in plants are mediated by ammonium transporters (AMTs), which are tightly regulated by phosphorylation to prevent excess ammonium influx and toxic accumulation. However, the mechanism of phosphorylation-mediated inactivation is unique and remains unclear. Here, we report Cryo-EM structures of the rice ( Oryza sativa) ammonium transporter OsAMT1;1 in its wild-type and phosphomimetic variant T452D states. OsAMT1;1 forms a stable homotrimer, with conserved motifs affirming a shared transport mechanism within the AMT/MEP/Rh superfamily. Our structural analysis reveals that T452D phosphomimetic stabilizes an intracellular salt-bridge network and maintains the channel in a closed state, in which the ICL5 loop positions the hydrophobic plug residue Leu360 near the cytoplasmic exit to occlude the channel exit and abolish complementation capacity. Our findings elucidate phosphorylation-induced inactivation mechanism for the plant AMT1 subfamily, providing a structural paradigm for the post-translational regulation of nutrient uptake.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MAERL accelerates atherosclerosis by inhibiting macrophage efferocytosis via transglutaminase 2. MAERL通过谷氨酰胺转酶2抑制巨噬细胞efferocytosis，从而加速动脉粥样硬化。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-10-14 DOI: 10.3724/abbs.2026092

Kun Xiao, Yajing Wang, Qianqian Wu, Zhenghao Zhang, Shujuan Li, Jiaqi Yang, Xiangyu Zhao, Guizhong Li, Jianmin Sun, Fang Ma, Shengchao Ma, Guodong Zhang

{"title":"MAERL accelerates atherosclerosis by inhibiting macrophage efferocytosis via transglutaminase 2.","authors":"Kun Xiao, Yajing Wang, Qianqian Wu, Zhenghao Zhang, Shujuan Li, Jiaqi Yang, Xiangyu Zhao, Guizhong Li, Jianmin Sun, Fang Ma, Shengchao Ma, Guodong Zhang","doi":"10.3724/abbs.2026092","DOIUrl":"https://doi.org/10.3724/abbs.2026092","url":null,"abstract":"Atherosclerotic cardiovascular and cerebrovascular diseases continue to represent the leading cause of global disease burden and mortality. Defective efferocytosis the phagocytic clearance of apoptotic cells by macrophages, is a well-established pathological mechanism that fuels chronic inflammation and drives necrotic core expansion in atherosclerotic plaques. Hyperhomocysteinemia (HHcy) is an independent risk factor for atherosclerosis development. However, the role of long non-coding RNAs (lncRNAs) induced by homocysteine (Hcy) in this process remains largely unexplored. Here, we demonstrate that Hcy impairs macrophage efferocytosis and enhances inflammation in atherosclerosis, both in high methionine diet (HMD)-fed ApoE -/- mice and in RAW264.7 cells treated with Hcy. We further identify a markedly up-regulated lncRNA in Hcy-induced macrophages, termed macrophage efferocytosis-related lncRNA (MAERL). Knockdown of MAERL attenuates the impairment of efferocytosis and reduces inflammation. Mechanistically, MAERL interacts with and inhibits transglutaminase 2 (TGM2), thereby significantly suppressing macrophage efferocytosis and promoting inflammation. Collectively, these findings reveal a MAERL/TGM2 pathway in macrophages as a key regulatory mechanism in the development of atherosclerosis.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sestrin2 mitigates obesity-associated HFpEF via adaptive IRE1α-XBP1 signaling and redox regulation. Sestrin2通过自适应IRE1α-XBP1信号和氧化还原调节减轻肥胖相关的HFpEF。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-10-10 DOI: 10.3724/abbs.2026168

Kexin Zhang, Chengxia Kan, Jingwen Zhang, Yujie Ma, Hongyan Qiu, Junfeng Shi, Sufang Sheng, Guoji Xiong, Ningning Hou, Fang Han, Xiaodong Sun

{"title":"Sestrin2 mitigates obesity-associated HFpEF via adaptive IRE1α-XBP1 signaling and redox regulation.","authors":"Kexin Zhang, Chengxia Kan, Jingwen Zhang, Yujie Ma, Hongyan Qiu, Junfeng Shi, Sufang Sheng, Guoji Xiong, Ningning Hou, Fang Han, Xiaodong Sun","doi":"10.3724/abbs.2026168","DOIUrl":"https://doi.org/10.3724/abbs.2026168","url":null,"abstract":"Obesity-associated heart failure with preserved ejection fraction (HFpEF) is a metabolic cardiac disorder characterized by diastolic dysfunction. Sestrin2 is a stress-inducible regulator of metabolic and redox homeostasis, but its role in HFpEF remains incompletely defined. This study demonstrates that Sestrin2 has cardioprotective effects on obesity-associated HFpEF. In an obesity-associated HFpEF mouse model, cardiac Sestrin2 overexpression attenuates diastolic dysfunction, myocardial lipid accumulation, fibrosis, hypertrophy, and mitochondrial dysfunction without significantly affecting adiposity, circulating lipid levels, or whole-body substrate utilization. Mechanistically, Sestrin2 overexpression increases IRE1α phosphorylation and XBP1 splicing, indicating enhanced adaptive unfolded protein response signaling. Sestrin2 overexpression is also associated with increased Sigma-1 receptor (Sigmar1) expression, whereas Sigmar1 knockdown attenuates Sestrin2-associated IRE1α-XBP1 activation in vitro, suggesting the involvement of Sigmar1 in endoplasmic reticulum-mitochondrial stress adaptation. In addition, Sestrin2 overexpression enhances AMPK activation, increases acetyl-CoA carboxylase (AAC) and eNOS phosphorylation, suppresses mTOR signaling, enhances Nrf2-HO-1 antioxidant responses, and reduces inflammatory marker expression and mitochondrial ROS production. Metabolomic analysis further reveals partial alterations in metabolites associated with endoplasmic reticulum stress and redox homeostasis. Collectively, these findings suggest that Sestrin2 alleviates obesity-associated HFpEF and is associated with the activation of adaptive IRE1α-XBP1 signaling involving Sigmar1, together with improved metabolic and redox homeostasis.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149163522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Intracellular COMP drives ovarian cancer progression through AKT/ERK signaling with concomitant pathway-dependent transgelin upregulation. 细胞内COMP通过AKT/ERK信号通路驱动卵巢癌进展，并伴随通路依赖的转胶蛋白上调。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-10-09 DOI: 10.3724/abbs.2026158

Yuxin Zhao, Junyi Zhang, Yingying Hu, Xiaolong Zhou, Ailing Gui, Yichen Yan, Jiule Ding, Ling Yang

引用次数: 0

Metabolic gene-based clustering identifies the role of acyl-CoA synthetase long-chain family member 1 in sepsis. 代谢基因聚类鉴定酰基辅酶a合成酶长链家族成员1在脓毒症中的作用。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-10-08 DOI: 10.3724/abbs.2026148

Dehao Zhu, Yinjiaozhi Li, Fan Wang, Yunqi Dai, Ranran Li, Yipeng Zhou, Chengcheng Shen, Tingting Pan, Hongping Qu, Ruoming Tan

{"title":"Metabolic gene-based clustering identifies the role of acyl-CoA synthetase long-chain family member 1 in sepsis.","authors":"Dehao Zhu, Yinjiaozhi Li, Fan Wang, Yunqi Dai, Ranran Li, Yipeng Zhou, Chengcheng Shen, Tingting Pan, Hongping Qu, Ruoming Tan","doi":"10.3724/abbs.2026148","DOIUrl":"https://doi.org/10.3724/abbs.2026148","url":null,"abstract":"Sepsis patients display substantial metabolic heterogeneity. Here, we classify sepsis patients into distinct metabolic clusters using transcriptomic profiles of metabolism-related genes, aiming to uncover key metabolic drivers of disease progression. Unsupervised clustering identifies three metabolic gene signature clusters (MGSC1, MGSC2, and MGSC3), with MGSC2 exhibiting the greatest disease severity and an activated fatty acid metabolism profile. Pathway enrichment analysis highlights MGSC2-specific metabolic dysregulation, and LightGBM-based feature selection identifies acyl-CoA synthetase long-chain family member 1 (ACSL1) as the hallmark gene of MGSC2, which is significantly upregulated in septic peripheral blood mononuclear cells (PBMCs). Molecular docking and in vitro assays demonstrate that osthole, a natural coumarin derivative, directly targets ACSL1, reducing lipid peroxidation and ferroptosis in septic PBMCs. Single-cell RNA sequencing reveals that ACSL1 is predominantly overexpressed in a pathogenic monocyte subset, driving sepsis progression. These findings suggest that metabolic stratification can distinguish clinically relevant subtypes of sepsis, with ACSL1 representing a key therapeutic target. Furthermore, osthole shows potential as a targeted intervention by inhibiting ACSL1-mediated ferroptosis in PBMCs from sepsis patients.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Integrated metabolomics and machine learning for coronary artery disease severity stratification: identification of plasma metabolic signatures. 冠状动脉疾病严重程度分层的综合代谢组学和机器学习：血浆代谢特征的识别。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-30 DOI: 10.3724/abbs.2026163

Ting Hu, Xian Ding, Feifei Han, Zhuoling An

{"title":"Integrated metabolomics and machine learning for coronary artery disease severity stratification: identification of plasma metabolic signatures.","authors":"Ting Hu, Xian Ding, Feifei Han, Zhuoling An","doi":"10.3724/abbs.2026163","DOIUrl":"https://doi.org/10.3724/abbs.2026163","url":null,"abstract":"Coronary artery disease (CAD) remains a leading cause of global mortality and morbidity. Current diagnostic methods, such as coronary angiography, are invasive and resource intensive. Metabolomics offers a powerful approach to identify disease-related metabolic signatures. This study aims to characterize plasma metabolic alterations in CAD patients and develop a biomarker panel for severity stratification. A total of 617 participants, including 297 healthy controls and 320 CAD patients, are classified by coronary angiography into mild (< 70% stenosis) and severe (≥ 70% stenosis) groups and further stratified by clinical presentation into asymptomatic, angina, and myocardial infarction subgroups. Untargeted metabolomics is performed on plasma samples. Differential metabolites are identified via statistical analysis, and machine learning models are developed to predict CAD severity. A total of 253 significantly altered metabolites are identified between CAD patients and controls, which are primarily involved in lipid metabolism, caffeine metabolism, amino acid metabolism, and energy pathways. Key metabolites such as caffeine show stepwise decreases with increasing CAD severity, while oxylipins exhibit progressive increases. Weighted gene co-expression network analysis (WGCNA) identifies 30 metabolic modules, with modules significantly correlated with CAD severity. Machine learning models integrating clinical and metabolomic data achieve high diagnostic accuracy, with area under the receiver operating characteristic curve (AUC) values > 0.95 for CAD stratification. Therefore, this study comprehensively characterizes plasma metabolic alterations in CAD and identifies potential biomarker panels for clinical stratification. The integration of metabolomics and machine learning shows promise for the early detection and personalized management of CAD.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Evolution, application and clinical significance of profiling chromatin interactions at a genome-wide scale. 全基因组染色质相互作用分析的进化、应用和临床意义。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-29 DOI: 10.3724/abbs.2026165

Qianqian Qian, Yanhui Xu, Lu Wei

{"title":"Evolution, application and clinical significance of profiling chromatin interactions at a genome-wide scale.","authors":"Qianqian Qian, Yanhui Xu, Lu Wei","doi":"10.3724/abbs.2026165","DOIUrl":"https://doi.org/10.3724/abbs.2026165","url":null,"abstract":"Over the past few decades, chromatin biology has evolved from viewing chromatin as a static structural scaffold to decoding it as a dynamic, programmable regulatory landscape. At the heart of this transformation is the precise mapping of interactions between functional proteins and cognate DNA elements. Although high-throughput technologies have generated comprehensive atlases of these genomic features, the field is now transitioning from descriptive mapping to mechanistic elucidation, paving the way for predictive diagnostics and target therapeutics. Here, we review the conceptual and methodological evolution of chromatin-protein interaction profiling, tracing the history from classical biochemical footprints to single-cell multi-omic integration. We reason that specific chromatin-protein interactions may serve as key structural linchpins organizing 3D genome architecture. By coupling single-cell multi-omics with functional perturbation, we illustrate how to move beyond observational correlations to establish direct causal links connecting chromatin architecture, epigenetic modifications, and transcriptional outputs. Ultimately, we conceptualize \"Sentinel Genomics\", an emerging paradigm leveraging these multi-layered chromatin insights to forecast disease trajectories and therapeutic responses well before clinical manifestation.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rbks plays a novel role in maintaining glycolipid metabolic homeostasis. Rbks在维持糖脂代谢稳态中起着新的作用。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-29 DOI: 10.3724/abbs.2026126

Zhongbin Yang, Houyu Li, Zeying Wang, Hongge Ju, Qi He, Liran He, Jingye Zhou, Caixia Shi, Feifei Zhu, Kun Hou, Lili Li, Zehong Zhang, Yu Tai, Qiang Ma, Xiaojing Li, Jing Jin, Zhi Liu, Yan Su

{"title":"Rbks plays a novel role in maintaining glycolipid metabolic homeostasis.","authors":"Zhongbin Yang, Houyu Li, Zeying Wang, Hongge Ju, Qi He, Liran He, Jingye Zhou, Caixia Shi, Feifei Zhu, Kun Hou, Lili Li, Zehong Zhang, Yu Tai, Qiang Ma, Xiaojing Li, Jing Jin, Zhi Liu, Yan Su","doi":"10.3724/abbs.2026126","DOIUrl":"https://doi.org/10.3724/abbs.2026126","url":null,"abstract":"Elevated urinary D-ribose has been observed in patients with diabetes and Alzheimer's disease, although the underlying mechanism remains unclear. Since ribokinase (Rbks) catalyzes the phosphorylation of D-ribose to ribose-5-phosphate, we hypothesize that the Rbks gene plays a crucial role in regulating systemic glucose and lipid metabolism. To test this hypothesis, we generate Rbks-knockout (KO) C57BL/6J mice using CRISPR/Cas9 and conduct a 16-week phenotypic observation. Although KO mice exhibit normal physical appearance and body weight, they show reduced food consumption and water intake. Serum levels of total cholesterol (T-CHO) and low-density lipoprotein cholesterol (LDL-C) are decreased, accompanied by hepatic accumulation of T-CHO. Proteomic analysis identifies 117 differentially expressed proteins associated with glycolipid metabolism and oxidative phosphorylation. Metabolomic profiling reveals 414 altered metabolites enrich in lipid metabolism, central carbon metabolism, and amino acid metabolism pathways. Among these alterations, the most prominent change is enhanced hepatic cholesterol and bile acid (BA) synthesis, which is supported by elevated hepatic T-CHO levels and increased mRNA expressions of 3-hydroxy-3-methylglutaryl-CoA reductase ( Hmgcr) and squalene epoxidase ( Sqle). This study reveals a novel role for Rbks in maintaining glucose-lipid metabolic homeostasis, especially with potential implications for understanding metabolic disorders characterized by altered cholesterol flux.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0