ArticleNature communications2022
GPSM1 impairs metabolic homeostasis by controlling a pro-inflammatory pathway in macrophages.
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Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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33citing papers in PubMed
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33 citing papers in PubMed, 42 citations in OpenAlex.
- Review
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- LncRNA Gm16023 limits M1 macrophage-mediated hyperglycemia-exacerbated septic intestinal injury via miR-377-3p/Sirt1 axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- The association of GNAS defects with pro-inflammatory adipokine levels in pseudohypoparathyroidism type 1.Journal of endocrinological investigation · 2026Article
- GPSM1 restricts CD73Nature communications · 2026Article
- Macrophage SH3 domain‑containing GRB2‑like protein B1 is required for Rab7‑mediated mitophagy in inflammation during sea water drowning acute lung injury.International journal of molecular medicine · 2026Article
- Neural impairments caused by energy storage material NCM811 via aberrated synaptic pruning: role of Th17 cells in microglia polarization.Journal of neuroinflammation · 2026Article
- Metabolic dysregulation reshapes the immune landscape: The gut microbiota-mTOR axis in respiratory viral infection immunity.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Review
- Engineered apoptotic vesicle mimetics with tunable "eat-me" signaling precisely regulate tumor-associated macrophages for potentiating cancer immunotherapy.Acta pharmaceutica Sinica. B · 2026Article
- An atlas of genetic effects on the monocyte methylome across European and African populations.Genome medicine · 2026Article
- Fibulin-7 in progenitor cells promotes adipose tissue fibrosis and disrupts metabolic homeostasis in obesity.Protein & cell · 2026Article
- Impact of sarcopenia and obesity on skeletal muscle size, gene expression, and mitochondrial function.GeroScience · 2026Article
- Myeloid GPSM1 regulates atherosclerosis progression by governing monocyte and macrophage activation and chemotaxis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Deletion of EP3 prostaglandin receptor in murine macrophages aggravates diet-induced obesity by suppressing SPARC.The EMBO journal · 2025Article
- Cardiometabolic Index as a predictor of mortality in metabolic Dysfunction-Associated Steatotic Liver Disease.BMC gastroenterology · 2025Article
- Novel anti-pyroptosis drug loaded on metal-organic framework for intervertebral disc degeneration therapy.Materials today. Bio · 2025Article
- A pretrained transformer model for decoding individual glucose dynamics from continuous glucose monitoring data.National science review · 2025Article
- Fam172a Mediates the Stimulation of Hypothalamic Oxytocin Neurons to Suppress Obesity-Induced Anxiety.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
21 authors at 3 institutions in 1 country.
Jing Yan *Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuemei Zhang *Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hairong Yu *Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yicen Zong *Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Daixi WangShanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jiangfei ZhengShanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Li JinShanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiangtian YuClinical Research Center, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Caizhi LiuShanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yi ZhangShanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Feng JiangShanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Rong ZhangShanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiangnan FangShanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ting XuDepartment of Bariatric and Metabolic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Mingyu LiMedicinal Chemistry and Bioinformatics Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jianzhong DiDepartment of Bariatric and Metabolic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yan LuInstitute of Metabolism and Regenerative Medicine, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-3468-2241
Xinran MaShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
Jian ZhangMedicinal Chemistry and Bioinformatics Center & Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-6558-791X
Weiping JiaShanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-6244-2168
Cheng HuShanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. alfredhc@sjtu.edu.cn.ORCID 0000-0003-4314-2386
Shanghai Jiao Tong University · CNEast China Normal University · CNXian Central Hospital · CN
Funding
No grant is acknowledged in the PubMed record.
Abstract
G-protein-signaling modulator 1 (GPSM1) exhibits strong genetic association with Type 2 diabetes (T2D) and Body Mass Index in population studies. However, how GPSM1 carries out such control and in which types of cells are poorly understood. Here, we demonstrate that myeloid GPSM1 promotes metabolic inflammation to accelerate T2D and obesity development. Mice with myeloid-specific GPSM1 ablation are protected against high fat diet-induced insulin resistance, glucose dysregulation, and liver steatosis via repression of adipose tissue pro-inflammatory states. Mechanistically, GPSM1 deficiency mainly promotes TNFAIP3 transcription via the Gα
Indexed as
Diabetes Mellitus, Type 2AnimalsGuanine Nucleotide Dissociation InhibitorsHomeostasisInflammationMacrophagesMiceMice, Inbred C57BLObesityGpsm1 protein, mouseGuanine Nucleotide Dissociation Inhibitors
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.