Pub Date : 2025-11-04DOI: 10.1016/j.cmet.2025.10.004
Kaylee Zilinger, Rachel J. Perry
Mechanisms that preserve glucose homeostasis are highly conserved across species, with the brain playing a central role in regulating these counterregulatory responses. However, the exact neural circuits underlying this regulation remain poorly understood. The previewed papers illuminate how the ventromedial hypothalamus orchestrates glycemic responses through brain-liver communication during periods of increased glucose demand.
{"title":"The role of the ventromedial hypothalamus in glycemic responses","authors":"Kaylee Zilinger, Rachel J. Perry","doi":"10.1016/j.cmet.2025.10.004","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.10.004","url":null,"abstract":"Mechanisms that preserve glucose homeostasis are highly conserved across species, with the brain playing a central role in regulating these counterregulatory responses. However, the exact neural circuits underlying this regulation remain poorly understood. The previewed papers illuminate how the ventromedial hypothalamus orchestrates glycemic responses through brain-liver communication during periods of increased glucose demand.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"112 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145434672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-04DOI: 10.1016/j.cmet.2025.10.002
Hanieh Yaghootkar
Emerging evidence challenges the view of obesity as a uniform metabolic risk. Spotlighting the recent Nature Medicine study by Chami et al.,1 this piece discusses how “uncoupling” adiposity from its cardiometabolic consequences reveals biologically distinct subtypes of obesity. Integrating imaging and multi-omics offers a promising path toward personalized obesity management and deeper mechanistic insight.
{"title":"When more is not worse: Genetic subtypes of obesity challenge conventional risk paradigms","authors":"Hanieh Yaghootkar","doi":"10.1016/j.cmet.2025.10.002","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.10.002","url":null,"abstract":"Emerging evidence challenges the view of obesity as a uniform metabolic risk. Spotlighting the recent <em>Nature Medicine</em> study by Chami et al.,<span><span><sup>1</sup></span></span> this piece discusses how “uncoupling” adiposity from its cardiometabolic consequences reveals biologically distinct subtypes of obesity. Integrating imaging and multi-omics offers a promising path toward personalized obesity management and deeper mechanistic insight.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"43 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145434673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-31DOI: 10.1016/j.cmet.2025.10.003
Maria-Kyriaki Drekolia, Janina Mettner, Daiyu Wang, Fredy Delgado Lagos, Christian Koch, Dennis Hecker, Jeanette Eresch, Yifang Mao, Marion Bähr, Dieter Weichenhan, Julio Cordero, Janina Wittig, Boran Zhang, Hanyu Cui, Xiaoming Li, James A. Oo, Andreas Weigert, Mauro Siragusa, Stephan Klatt, Ingrid Fleming, Sofia-Iris Bibli
Endothelial metabolism underpins tissue regeneration, health, and longevity. We uncover a nuclear oxidative catabolic pathway linking cystine to gene regulation. Cells preparing to proliferate upregulate the SLC7A11 transporter to import cystine, which is oxidatively catabolized by cystathionine-γ-lyase (CSE) in the nucleus. This generates acetyl units via pyruvate dehydrogenase, driving site-specific histone H3 acetylation and chromatin remodeling that sustain endothelial transcription and proliferation. Combined loss of SLC7A11 and CSE abolishes cystine oxidative and reductive metabolism and causes embryonic lethality, whereas single deletions reveal distinct effects. SLC7A11 deficiency triggers compensatory cysteine de novo biosynthesis, partially maintaining angiogenesis, while CSE deletion disrupts nuclear cystine oxidative catabolism, transcription, and vessel formation. Therapeutically, cystine supplementation promotes vascular repair in retinopathy of prematurity, myocardial infarction, and injury in aging. These findings establish the role of cystine nuclear oxidative catabolism as a fundamental metabolic axis coupling nutrient utilization to gene regulation, with implications for vascular regeneration.
{"title":"Cystine import and oxidative catabolism fuel vascular growth and repair via nutrient-responsive histone acetylation","authors":"Maria-Kyriaki Drekolia, Janina Mettner, Daiyu Wang, Fredy Delgado Lagos, Christian Koch, Dennis Hecker, Jeanette Eresch, Yifang Mao, Marion Bähr, Dieter Weichenhan, Julio Cordero, Janina Wittig, Boran Zhang, Hanyu Cui, Xiaoming Li, James A. Oo, Andreas Weigert, Mauro Siragusa, Stephan Klatt, Ingrid Fleming, Sofia-Iris Bibli","doi":"10.1016/j.cmet.2025.10.003","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.10.003","url":null,"abstract":"Endothelial metabolism underpins tissue regeneration, health, and longevity. We uncover a nuclear oxidative catabolic pathway linking cystine to gene regulation. Cells preparing to proliferate upregulate the SLC7A11 transporter to import cystine, which is oxidatively catabolized by cystathionine-γ-lyase (CSE) in the nucleus. This generates acetyl units via pyruvate dehydrogenase, driving site-specific histone H3 acetylation and chromatin remodeling that sustain endothelial transcription and proliferation. Combined loss of SLC7A11 and CSE abolishes cystine oxidative and reductive metabolism and causes embryonic lethality, whereas single deletions reveal distinct effects. SLC7A11 deficiency triggers compensatory cysteine <em>de novo</em> biosynthesis, partially maintaining angiogenesis, while CSE deletion disrupts nuclear cystine oxidative catabolism, transcription, and vessel formation. Therapeutically, cystine supplementation promotes vascular repair in retinopathy of prematurity, myocardial infarction, and injury in aging. These findings establish the role of cystine nuclear oxidative catabolism as a fundamental metabolic axis coupling nutrient utilization to gene regulation, with implications for vascular regeneration.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"67 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145404394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-16DOI: 10.1016/j.cmet.2025.09.009
Connor S.R. Jankowski, Laith Z. Samarah, Michael R. MacArthur, Sarah J. Mitchell, Daniel R. Weilandt, Craig J. Hunter, Xianfeng Zeng, Melanie R. McReynolds, Joshua D. Rabinowitz
Metabolic dysregulation is a hallmark of aging. Here, we investigate in mice age-induced metabolic alterations using metabolomics and stable isotope tracing. Circulating metabolite fluxes and serum and tissue concentrations were measured in young and old (20–30 months) C57BL/6J mice, with young obese (ob/ob) mice as a comparator. For major circulating metabolites, concentrations changed more with age than fluxes, and fluxes changed more with obesity than with aging. Specifically, glucose, lactate, 3-hydroxybutryate, and many amino acids (but notably not taurine) change significantly in concentration with age. Only glutamine circulatory flux does so. The fluxes of major circulating metabolites remain stable despite underlying metabolic changes. For example, lysine catabolism shifts from the saccharopine toward the pipecolic acid pathway, and both pipecolic acid concentration and flux increase with aging. Other less-abundant metabolites also show coherent, age-induced concentration and flux changes. Thus, while aging leads to widespread metabolic changes, major metabolic fluxes are largely preserved.
{"title":"Aged mice exhibit widespread metabolic changes but preserved major fluxes","authors":"Connor S.R. Jankowski, Laith Z. Samarah, Michael R. MacArthur, Sarah J. Mitchell, Daniel R. Weilandt, Craig J. Hunter, Xianfeng Zeng, Melanie R. McReynolds, Joshua D. Rabinowitz","doi":"10.1016/j.cmet.2025.09.009","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.09.009","url":null,"abstract":"Metabolic dysregulation is a hallmark of aging. Here, we investigate in mice age-induced metabolic alterations using metabolomics and stable isotope tracing. Circulating metabolite fluxes and serum and tissue concentrations were measured in young and old (20–30 months) C57BL/6J mice, with young obese (ob/ob) mice as a comparator. For major circulating metabolites, concentrations changed more with age than fluxes, and fluxes changed more with obesity than with aging. Specifically, glucose, lactate, 3-hydroxybutryate, and many amino acids (but notably not taurine) change significantly in concentration with age. Only glutamine circulatory flux does so. The fluxes of major circulating metabolites remain stable despite underlying metabolic changes. For example, lysine catabolism shifts from the saccharopine toward the pipecolic acid pathway, and both pipecolic acid concentration and flux increase with aging. Other less-abundant metabolites also show coherent, age-induced concentration and flux changes. Thus, while aging leads to widespread metabolic changes, major metabolic fluxes are largely preserved.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"24 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145295524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-15DOI: 10.1016/j.cmet.2025.09.008
Joseph Longo, McLane J. Watson, Kelsey S. Williams, Ryan D. Sheldon, Russell G. Jones
T cell activation and function are intricately linked to metabolic reprogramming. The classic view of T cell metabolic reprogramming centers on glucose as the dominant bioenergetic fuel, where T cell receptor (TCR) stimulation promotes a metabolic switch from relying primarily on oxidative phosphorylation (OXPHOS) for energy production to aerobic glycolysis (i.e., the Warburg effect). More recently, studies have revealed this classic model to be overly simplistic. Activated T cells run both glycolysis and OXPHOS programs concurrently, allocating diverse nutrient sources toward distinct biosynthetic and bioenergetic fates. Moreover, studies of T cell metabolism in vivo and ex vivo highlight that physiologic nutrient availability influences how glucose is allocated by T cells to fuel both optimal proliferation and effector function. Here, we summarize recent advancements that support a revised model of effector T cell metabolism, where strategic nutrient allocation fuels optimal T cell-mediated immunity.
{"title":"Nutrient allocation fuels T cell-mediated immunity","authors":"Joseph Longo, McLane J. Watson, Kelsey S. Williams, Ryan D. Sheldon, Russell G. Jones","doi":"10.1016/j.cmet.2025.09.008","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.09.008","url":null,"abstract":"T cell activation and function are intricately linked to metabolic reprogramming. The classic view of T cell metabolic reprogramming centers on glucose as the dominant bioenergetic fuel, where T cell receptor (TCR) stimulation promotes a metabolic switch from relying primarily on oxidative phosphorylation (OXPHOS) for energy production to aerobic glycolysis (i.e., the Warburg effect). More recently, studies have revealed this classic model to be overly simplistic. Activated T cells run both glycolysis and OXPHOS programs concurrently, allocating diverse nutrient sources toward distinct biosynthetic and bioenergetic fates. Moreover, studies of T cell metabolism <em>in vivo</em> and <em>ex vivo</em> highlight that physiologic nutrient availability influences how glucose is allocated by T cells to fuel both optimal proliferation and effector function. Here, we summarize recent advancements that support a revised model of effector T cell metabolism, where strategic nutrient allocation fuels optimal T cell-mediated immunity.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"71 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145289269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The brain relies heavily on glucose for energy resources, and thus prompt counterregulatory responses to hypoglycemia in connection with glucose production are fundamental. We identified a biphasic pattern in blood and hypothalamic glucose dynamics during prolonged fasting, revealing an additional threshold-dependent mechanism for counterregulation. This mechanism is mediated by a ventromedial hypothalamus (VMH)→paraventricular hypothalamic nucleus (PVH)→lateral paragigantocellular nucleus (LPGi)→liver neurocircuit that detects neuroglycopenia and transmits neural signals to drive hepatic glucose production via intrahepatic sympathetic activation. Using viral tracing, single-nucleus RNA sequencing, and various unbiased methods, we identified Galnt2 as both a genetic marker and molecular brake of VMH glucose-inhibited neurons, modulating the glycemic threshold for hypoglycemia perception and metabolic homeostasis. Our results highlight a VMHGalnt2-originated brain-liver neurocircuit that perceives and counterregulates hypoglycemia and may pave the way to innovative therapeutic strategies against metabolic disorders characterized by glucose dysregulation.
{"title":"Galnt2 neurons in the ventromedial hypothalamus counterregulate hypoglycemia via a brain-liver neurocircuit","authors":"Junjie Wang, Xinyuan Sun, Xiangfei Gong, Wenling Dai, Hao Hong, Li Jiang, Zhonglong Wang, Zhiyuan Tang, Xiaobo Wu, Peng Sun, Yongjie Zhang, Kun Hao, Fang Zhou, Ying Cui, Tianyu Tang, Xiao Zheng, Lanqun Mao, Guangji Wang, Haiping Hao, Hao Xie","doi":"10.1016/j.cmet.2025.09.006","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.09.006","url":null,"abstract":"The brain relies heavily on glucose for energy resources, and thus prompt counterregulatory responses to hypoglycemia in connection with glucose production are fundamental. We identified a biphasic pattern in blood and hypothalamic glucose dynamics during prolonged fasting, revealing an additional threshold-dependent mechanism for counterregulation. This mechanism is mediated by a ventromedial hypothalamus (VMH)→paraventricular hypothalamic nucleus (PVH)→lateral paragigantocellular nucleus (LPGi)→liver neurocircuit that detects neuroglycopenia and transmits neural signals to drive hepatic glucose production via intrahepatic sympathetic activation. Using viral tracing, single-nucleus RNA sequencing, and various unbiased methods, we identified Galnt2 as both a genetic marker and molecular brake of VMH glucose-inhibited neurons, modulating the glycemic threshold for hypoglycemia perception and metabolic homeostasis. Our results highlight a VMH<sup>Galnt2</sup>-originated brain-liver neurocircuit that perceives and counterregulates hypoglycemia and may pave the way to innovative therapeutic strategies against metabolic disorders characterized by glucose dysregulation.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"18 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145283559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-10DOI: 10.1016/j.cmet.2025.09.015
Artem Khan, Frederick S. Yen, Gokhan Unlu, Nicole L. DelGaudio, Ranya Erdal, Michael Xiao, Khando Wangdu, Kevin Cho, Eric R. Gamazon, Gary J. Patti, Kıvanç Birsoy
Solute carriers (SLCs) regulate cellular and organismal metabolism by transporting small molecules and ions across membranes, yet the physiological substrates of ∼20% remain elusive. To address this, we developed a machine-learning platform to predict gene-metabolite associations. This approach identifies UNC93A and SLC45A4 as candidate plasma membrane transporters for acetylglucosamine and polyamines, respectively. Additionally, we uncover SLC25A45 as a mitochondrial transporter linked to serum levels of methylated basic amino acids, products of protein catabolism. Mechanistically, SLC25A45 is necessary for the mitochondrial import of methylated basic amino acids, including ADMA and TML, the latter serving as a precursor for carnitine synthesis. In line with this observation, SLC25A45 loss impairs carnitine synthesis and blunts upregulation of carnitine-containing metabolites under fasted conditions. By facilitating mitochondrial TML import, SLC25A45 connects protein catabolism to carnitine production, sustaining β-oxidation during fasting. Altogether, our study identifies putative substrates for three SLCs and provides a resource for transporter deorphanization.
{"title":"Machine-learning-guided discovery of SLC25A45 as a mediator of mitochondrial methylated amino acid import and carnitine synthesis","authors":"Artem Khan, Frederick S. Yen, Gokhan Unlu, Nicole L. DelGaudio, Ranya Erdal, Michael Xiao, Khando Wangdu, Kevin Cho, Eric R. Gamazon, Gary J. Patti, Kıvanç Birsoy","doi":"10.1016/j.cmet.2025.09.015","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.09.015","url":null,"abstract":"Solute carriers (SLCs) regulate cellular and organismal metabolism by transporting small molecules and ions across membranes, yet the physiological substrates of ∼20% remain elusive. To address this, we developed a machine-learning platform to predict gene-metabolite associations. This approach identifies UNC93A and SLC45A4 as candidate plasma membrane transporters for acetylglucosamine and polyamines, respectively. Additionally, we uncover SLC25A45 as a mitochondrial transporter linked to serum levels of methylated basic amino acids, products of protein catabolism. Mechanistically, SLC25A45 is necessary for the mitochondrial import of methylated basic amino acids, including ADMA and TML, the latter serving as a precursor for carnitine synthesis. In line with this observation, SLC25A45 loss impairs carnitine synthesis and blunts upregulation of carnitine-containing metabolites under fasted conditions. By facilitating mitochondrial TML import, SLC25A45 connects protein catabolism to carnitine production, sustaining β-oxidation during fasting. Altogether, our study identifies putative substrates for three SLCs and provides a resource for transporter deorphanization.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"37 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145254946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-07DOI: 10.1016/j.cmet.2025.09.005
Joanne F. Garbincius, John W. Elrod
The mechanisms mediating calcium transport into and out of the mitochondrial matrix have critical implications for signaling, bioenergetics, and cell death. Zhang et al.1 propose that the protein TMEM65, recently identified as a key component of the mitochondrial calcium efflux machinery, functions as the mitochondrial sodium/calcium exchanger. Their report encourages critical re-examination of the components required for mitochondrial calcium handling.
{"title":"Mitochondrial sodium-calcium exchange—Can TMEM65 do it alone?","authors":"Joanne F. Garbincius, John W. Elrod","doi":"10.1016/j.cmet.2025.09.005","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.09.005","url":null,"abstract":"The mechanisms mediating calcium transport into and out of the mitochondrial matrix have critical implications for signaling, bioenergetics, and cell death. Zhang et al.<span><span><sup>1</sup></span></span> propose that the protein TMEM65, recently identified as a key component of the mitochondrial calcium efflux machinery, functions as the mitochondrial sodium/calcium exchanger. Their report encourages critical re-examination of the components required for mitochondrial calcium handling.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"83 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145241384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-07DOI: 10.1016/j.cmet.2025.09.007
Huixian Li, Daniel Mucida
The gut conveys nutritional, mechanical, and microbial signals to the brain to regulate physiology and behavior. Writing in Nature, Liu et al. reveal a colonic neuropod-vagus circuit that senses bacterial flagellin, highlighting microbial input as a rapid driver of feeding control and expanding paradigms of communication between the gut and the brain.
{"title":"An “electric” microbial cue to control food intake behavior","authors":"Huixian Li, Daniel Mucida","doi":"10.1016/j.cmet.2025.09.007","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.09.007","url":null,"abstract":"The gut conveys nutritional, mechanical, and microbial signals to the brain to regulate physiology and behavior. Writing in <em>Nature</em>, Liu et al. reveal a colonic neuropod-vagus circuit that senses bacterial flagellin, highlighting microbial input as a rapid driver of feeding control and expanding paradigms of communication between the gut and the brain.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"5 7 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145241312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-07DOI: 10.1016/j.cmet.2025.08.006
Xiangqi Chen, Xiaoqiang Tang, Yanping Li, Jinhan He
Atherosclerosis remains the leading type of cardiovascular disease, yet its pathogenesis is not completely understood, hindering the development of effective early diagnostics and therapeutics. Recent work by Mastrangelo et al. in Nature has identified a novel driver of atherosclerosis, the gut microbiota-derived metabolite imidazole propionate, which triggers atherosclerosis via the imidazoline-1 receptor in myeloid cells.
{"title":"Imidazole propionate: Cause and cure in atherosclerosis?","authors":"Xiangqi Chen, Xiaoqiang Tang, Yanping Li, Jinhan He","doi":"10.1016/j.cmet.2025.08.006","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.08.006","url":null,"abstract":"Atherosclerosis remains the leading type of cardiovascular disease, yet its pathogenesis is not completely understood, hindering the development of effective early diagnostics and therapeutics. Recent work by Mastrangelo et al. in <em>Nature</em> has identified a novel driver of atherosclerosis, the gut microbiota-derived metabolite imidazole propionate, which triggers atherosclerosis via the imidazoline-1 receptor in myeloid cells.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"59 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145241313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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