Cell metabolism最新文献_第2页

Lactate suppresses STING activation to promote tumor immune evasion. 乳酸抑制STING激活，促进肿瘤免疫逃逸。

IF 30.9

Cell metabolism Pub Date : 2026-09-01 DOI: 10.1016/j.cmet.2026.08.008

Yuan Tian, Xin Cai

引用次数: 0

Circadian Clock Interaction with HIF1α Mediates Oxygenic Metabolism and Anaerobic Glycolysis in Skeletal Muscle. 生物钟与HIF1α的相互作用介导骨骼肌的氧代谢和无氧糖酵解。

IF 30.9

Cell metabolism Pub Date : 2026-09-01 Epub Date: 2026-07-24 DOI: 10.1016/j.cmet.2026.07.017

Clara Bien Peek, Daniel C Levine, Jonathan Cedernaes, Akihiko Taguchi, Yumiko Kobayashi, Stacy J Tsai, Nicolle A Bonar, Maureen R McNulty, Kathryn Moynihan Ramsey, Joseph Bass

引用次数: 0

Pro-aging effects of chronic glucocorticoid signaling. 慢性糖皮质激素信号的促衰老作用。

IF 30.9

Cell metabolism Pub Date : 2026-09-01 Epub Date: 2026-05-28 DOI: 10.1016/j.cmet.2026.05.002

Flavia Lambertucci, Frederic Castinetti, Isabelle Martins, Carlos López-Otín, Guido Kroemer

{"title":"Pro-aging effects of chronic glucocorticoid signaling.","authors":"Flavia Lambertucci, Frederic Castinetti, Isabelle Martins, Carlos López-Otín, Guido Kroemer","doi":"10.1016/j.cmet.2026.05.002","DOIUrl":"10.1016/j.cmet.2026.05.002","url":null,"abstract":"Glucocorticoids (GCs) are essential endocrine regulators coordinating stress responsiveness, metabolic flexibility, inflammatory resolution, and circadian physiology. While acute GC fluctuations are adaptive, sustained exposure (arising from psychosocial stress, circadian disruption, obesity, chronic inflammation, neoplasms, or steroid therapy) elicits pleiotropic effects that overlap with biological aging. Prolonged GC signaling intersects with multiple hallmarks of aging by altering nutrient sensing, suppressing autophagy, impairing mitochondrial quality control, and promoting cellular senescence. In this context, the GC-responsive polypeptide ACBP/DBI (acyl-coenzyme A [CoA]-binding protein/diazepam-binding inhibitor) has emerged as a stress-induced inhibitor of macroautophagy that amplifies several metabolic and immune consequences of GC excess linked to aging phenotypes. Clinically, chronic GC elevation is associated with earlier and more severe manifestations of age-related diseases, including metabolic syndrome, osteoporosis, sarcopenia, neurodegeneration, cardiovascular disease, immunosenescence, and cancer. Here, we review mechanistic links between GC signaling and systemic aging and discuss strategies to mitigate the age-accelerating consequences of persistent GC exposure.","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":"1764-1785"},"PeriodicalIF":30.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148058858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An early-life window of opportunity opened by hyocholic acids. 胆酸打开了早期生命的机会之窗。

IF 30.9

Cell metabolism Pub Date : 2026-09-01 DOI: 10.1016/j.cmet.2026.07.003

Mary Elizabeth M Tessier, Geoffrey A Preidis

引用次数: 0

Dual targeting of SLC25A51 and succinate dehydrogenase selectively depletes mitochondrial NAD⁺ to eradicate KRAS-driven AML. SLC25A51和琥珀酸脱氢酶的双重靶向选择性地消耗线粒体NAD+以根除kras驱动的AML。

IF 30.9

Cell metabolism Pub Date : 2026-09-01 Epub Date: 2026-08-05 DOI: 10.1016/j.cmet.2026.07.026

Ang Jia, Xiaowen Zhang, Ji-Hao Zhou, Yongcan Ma, Jing Wang, Yongbo Gong, Wenjie Song, Hangcheng Hu, Yufei Yu, Haixia Yang, Youli Lu, Linzhang Huang, Xingrong Du, Chunmei Chang, Shanshan Pei, Peng Li, Craig T Jordan, Tong-Jin Zhao, Haobin Ye

引用次数: 0

Gut microbiota-derived lysine phenylacetylation impairs mitochondrial function and is alleviated by SIRT3. 肠道微生物来源的赖氨酸苯乙酰化损害线粒体功能，并通过SIRT3减轻。

IF 30.9

Cell metabolism Pub Date : 2026-09-01 Epub Date: 2026-06-24 DOI: 10.1016/j.cmet.2026.05.016

Wei Du, Jun-Yu Xu, Yufeng Li, Mingya Zhang, Yidan Huang, Shaoqian Zhao, Ying Zhou, Lei Zhao, Kexin Xu, Linhui Zhai, Wensi Zhao, Jia Liu, Jiahui Ni, Junxiao Dai, Tianxian Liu, Jie Hong, Haowen Jiang, Shuliang Zhao, Jian Zhang, Lu Zhou, Ji-Qiu Wang, Bin-Cheng Yin, Rui-Xin Liu, Jingya Li, Bang-Ce Ye, Minjia Tan

{"title":"Gut microbiota-derived lysine phenylacetylation impairs mitochondrial function and is alleviated by SIRT3.","authors":"Wei Du, Jun-Yu Xu, Yufeng Li, Mingya Zhang, Yidan Huang, Shaoqian Zhao, Ying Zhou, Lei Zhao, Kexin Xu, Linhui Zhai, Wensi Zhao, Jia Liu, Jiahui Ni, Junxiao Dai, Tianxian Liu, Jie Hong, Haowen Jiang, Shuliang Zhao, Jian Zhang, Lu Zhou, Ji-Qiu Wang, Bin-Cheng Yin, Rui-Xin Liu, Jingya Li, Bang-Ce Ye, Minjia Tan","doi":"10.1016/j.cmet.2026.05.016","DOIUrl":"10.1016/j.cmet.2026.05.016","url":null,"abstract":"Disturbances in the gut microbiota (GM) contribute to the pathogenesis of various prevalent metabolic disorders. Short-chain fatty acids act as signaling molecules and donors for host post-translational modifications. Here, we report a novel type of lysine modification, phenylacetylation (Kpaa), derived from the phenylalanine-dependent phenylacetic acid (PAA) metabolic pathway of the GM. Hepatic Kpaa levels were significantly elevated in mice with high-fat-diet-induced obesity and were reduced by the deacetylase sirtuin 3 (SIRT3). Proteome-wide substrates were significantly associated with mitochondria. PAA disrupted mitochondrial function and impaired insulin signaling. Mechanistically, PAA-induced K481paa of HSP60 triggered the mitochondrial unfolded protein response, which could be reversed by SIRT3. Finally, relatively low levels of hepatic SIRT3 in adults with obesity and metabolic dysfunction-associated steatohepatitis (MASH) were negatively correlated with increased Kpaa levels. Together, our study uncovered a microbiota-derived lysine acylation modification underlying its biological relevance in the development of metabolic dysfunction-associated steatotic liver disease (MASLD)/MASH.","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":"1864-1880.e8"},"PeriodicalIF":30.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148321114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Enhanced non-enzymatic H₂S generation extends lifespan and healthspan in male mice. 增强非酶促H2S生成延长雄性小鼠的寿命和健康寿命。

IF 30.9

Cell metabolism Pub Date : 2026-09-01 Epub Date: 2026-07-22 DOI: 10.1016/j.cmet.2026.07.014

María Ángeles Cáliz-Molina, Raúl López-Fernández-Sobrino, Inmaculada Pino-Pérez, Concepción Panadero-Morón, María Del Carmen Vilches-Pérez, María Camacho-Cabrera, Almudena García-Ruiz, Leopoldo Pérez-Rosendo, Isabel Espadas, Alejandro Sola-García, Mario Soriano-Navarro, Franz Martin, Mónica Venegas-Calerón, Joaquín Jesús Salas, Enrique Martínez-Force, Luis C Romero, Ángeles Aroca, Román González-Prieto, Máximo Bernabeu-Wittel, Vivian Capilla-González, Christopher Hine, Alejandro Martín-Montalvo

引用次数: 0

Brown fat protects against hepatic oxidative stress by remodeling the circulating metabolome. 棕色脂肪通过重塑循环代谢组来防止肝脏氧化应激。

IF 30.9

Cell metabolism Pub Date : 2026-09-01 Epub Date: 2026-07-14 DOI: 10.1016/j.cmet.2026.06.020

Dandan Wang, Mark Li, Tian Lu, Mami Matsushita, Juro Sakai, Masayuki Saito, Takeshi Yoneshiro, Shingo Kajimura

{"title":"Brown fat protects against hepatic oxidative stress by remodeling the circulating metabolome.","authors":"Dandan Wang, Mark Li, Tian Lu, Mami Matsushita, Juro Sakai, Masayuki Saito, Takeshi Yoneshiro, Shingo Kajimura","doi":"10.1016/j.cmet.2026.06.020","DOIUrl":"10.1016/j.cmet.2026.06.020","url":null,"abstract":"Brown adipose tissue (BAT) regulates systemic metabolism beyond thermogenesis, yet the circulating mediators through which BAT communicates with other organs remain less explored. Here, we performed comprehensive serum metabolomics and lipidomics in BAT-ablated mice and human cohorts with varying BAT activity to delineate how BAT activity shapes the circulating metabolome. By integrating datasets across serum, tissues, extracellular fluids, and conditioned media, we assembled BAT-linked circulating molecular signatures. The analyses support a critical role for BAT in the clearance of circulating branched-chain amino acids and triglycerides. We also identified a cold-inducible metabolite, 3-hydroxystearic acid (3-OHSA), produced primarily by BAT and released into circulation. 3-OHSA serves as a circulating readout of cold-activated BAT and acts on the liver to reduce mitochondrial membrane potential and reactive oxygen species production, thereby limiting oxidative stress. This work provides a framework for identifying BAT-derived mediators and uncovers a BAT-liver axis that coordinates adaptation to metabolic stress.","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":"1881-1895.e8"},"PeriodicalIF":30.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13440245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The senescence-stiffening loop: Extracellular matrix remodeling, hypoperfusion, and mitochondrial dysfunction drive tissue aging. 衰老-硬化循环：细胞外基质重塑、灌注不足和线粒体功能障碍驱动组织衰老。

IF 30.9

Cell metabolism Pub Date : 2026-09-01 Epub Date: 2026-06-15 DOI: 10.1016/j.cmet.2026.05.008

Luigi Ferrucci, Stefano Donega, Allison B Herman, Rafael de Cabo, Myriam Gorospe

{"title":"The senescence-stiffening loop: Extracellular matrix remodeling, hypoperfusion, and mitochondrial dysfunction drive tissue aging.","authors":"Luigi Ferrucci, Stefano Donega, Allison B Herman, Rafael de Cabo, Myriam Gorospe","doi":"10.1016/j.cmet.2026.05.008","DOIUrl":"10.1016/j.cmet.2026.05.008","url":null,"abstract":"Aging tissues experience a gradual decline in perfusion and metabolic resilience due to complex interactions among extracellular matrix (ECM) remodeling, vascular dysfunction, and mitochondrial impairment. Stiffening of the ECM that results from collagen crosslinking, elastin loss, and basement membrane thickening reduces vascular compliance and impairs local angiogenesis. The consequent reduction in capillaries and diminished endothelial reactivity leads to ongoing or intermittent hypoxia, which triggers changes in transcriptomic and proteomic programs that inhibit oxidative phosphorylation and facilitate the production of reactive oxygen species. Under these conditions, mitochondria produce less ATP than is needed for homeostatic repair. This energetic breakdown triggers cellular senescence and inflammation, further increasing ECM stiffening, and thus creating a self-sustaining feedback loop that accelerates tissue aging and functional decline. Such a continuum from ECM stiffening to mitochondrial dysfunction may be considered a new therapeutic target for strategies aimed at maintaining vascular integrity, mitochondrial health, and cellular homeostasis during aging.","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":"1754-1763"},"PeriodicalIF":30.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13336314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148260775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Maternal vitamin B12 deprivation exacerbates offspring obesity by reducing early-life colonization with Bifidobacterium pseudolongum. 母体维生素B12缺乏通过减少生命早期假结肠双歧杆菌的定植而加剧后代肥胖。

IF 30.9

Cell metabolism Pub Date : 2026-09-01 Epub Date: 2026-07-21 DOI: 10.1016/j.cmet.2026.06.022

Zhaoyi Liu, Xiuwen Yang, Huaili Feng, Ting You, Fanwei Sun, Jianjiang Xue, Weijuan Liang, Jinwen Yao, Yi Liao, Yanan Gao, Yuanjun Yang, Xuejun Jiang, Qiang Zhang, Zhen Zou, Jun Zhang, Xinhao Duan, Jiao Wang, Qian Chen, Peng Su, Shangcheng Xu, Jingfu Qiu, Chengzhi Chen

{"title":"Maternal vitamin B12 deprivation exacerbates offspring obesity by reducing early-life colonization with Bifidobacterium pseudolongum.","authors":"Zhaoyi Liu, Xiuwen Yang, Huaili Feng, Ting You, Fanwei Sun, Jianjiang Xue, Weijuan Liang, Jinwen Yao, Yi Liao, Yanan Gao, Yuanjun Yang, Xuejun Jiang, Qiang Zhang, Zhen Zou, Jun Zhang, Xinhao Duan, Jiao Wang, Qian Chen, Peng Su, Shangcheng Xu, Jingfu Qiu, Chengzhi Chen","doi":"10.1016/j.cmet.2026.06.022","DOIUrl":"10.1016/j.cmet.2026.06.022","url":null,"abstract":"Vitamin B12 deficiency during pregnancy and lactation is common, yet its mechanistic impact on reproductive outcomes and offspring health remains poorly understood. Here, we show that maternal dietary vitamin B12 deprivation not only impairs maternal glucose metabolism and reproductive outcomes but also exacerbates high-fat-diet-induced obesity in offspring. These effects are mediated by gut microbiota and associated with a marked reduction of Bifidobacterium pseudolongum (B. pseudolongum) in both dams and their offspring. Maternal vitamin B12 deprivation limits early-life acquisition of B. pseudolongum in offspring during lactation, subsequently intensifying obesity and metabolic dysregulation. Early-life restoration of B. pseudolongum or its key metabolite, acetate, effectively ameliorates this aggravated obesity. Mechanistically, acetate acts through the Ffar2 receptor to upregulate Ehhadh expression. Together, these data establish that perinatal nutrition imprints long-term metabolic phenotypes in offspring via early-life acquisition of the gut microbiota, with a critical window during lactation.","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":" ","pages":"1848-1863.e10"},"PeriodicalIF":30.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148551665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0