ArticleCellular & molecular immunology2021
Activation of AMPKα1 is essential for regulatory T cell function and autoimmune liver disease prevention.
Article in Cellular & molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Dysregulation of the AMPK-SREBP1-FASN axis in MASLD: driving a vicious cycle of lipotoxicity and metabolic-immune crosstalk.Lipids in health and disease · 2026Review
- Treg dysregulation in the oxidative lung milieu: an emerging mechanistic link in interstitial lung disease associated with systemic autoimmune rheumatic diseases.Frontiers in immunology · 2026Review
- Immune crosstalk in metabolic dysfunction-associated steatotic liver disease: interactions between innate and adaptive immunity.Frontiers in immunology · 2026Review
- Kinase signaling in the control of regulatory T cell function: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Lipid Metabolism in Regulatory T Cells in Health and Disease.Journal of inflammation research · 2026Review
- Regulatory T cells in bullous pemphigoid: biological characteristics, dysfunction, and pathogenic roles.Frontiers in immunology · 2026Review
- Can we cure autoimmune hepatitis?Current opinion in immunology · 2025Review
- AMPK in Intestinal Health and Disease: A Multifaceted Therapeutic Target for Metabolic and Inflammatory Disorders.Drug design, development and therapy · 2025Review
- Immunocyte lipid metabolic reprogramming: a novel pathway for targeted intervention in autoimmune diseases.Frontiers in immunology · 2025Review
- Unveiling the Role of GRK2: From Immune Regulation to Cancer Therapeutics.Mediators of inflammation · 2025Review
- Remote Ischemic Post-Conditioning (RIC) Mediates Anti-Inflammatory Signaling via Myeloid AMPKα1 in Murine Traumatic Optic Neuropathy (TON).International journal of molecular sciences · 2024Article
- Complex Interplay Between Metabolism and CD4Cardiovascular drugs and therapy · 2024Review
- PRKAG2.2 is essential for FoxA1Science advances · 2023Article
- Chronic inflammation and the hallmarks of aging.Molecular metabolism · 2023Review
- Review
- Ongoing involvers and promising therapeutic targets of hepatic fibrosis: The hepatic immune microenvironment.Frontiers in immunology · 2023Review
- Mechanism-based target therapy in primary biliary cholangitis: opportunities before liver cirrhosis?Frontiers in immunology · 2023Review
- The role of AMP-activated protein kinase in GVHD-causing T cells.Immunometabolism (Cobham, Surrey) · 2022Review
- Challenges and opportunities in achieving effective regulatory T cell therapy in autoimmune liver disease.Seminars in immunopathology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Regulatory T cells (Treg cells) are crucial for maintaining immune tolerance. Compromising the regulatory function of Treg cells can lead to autoimmune liver disease. However, how Treg cell function is regulated has not been fully clarified. Here, we report that mice with AMP-activated protein kinase alpha 1 (AMPKα1) globally knocked out spontaneously develop immune-mediated liver injury, with massive lymphocyte infiltration in the liver, elevated serum alanine aminotransferase levels, and greater production of autoantibodies. Both transplantation of wild-type bone marrow and adoptive transfer of wild-type Treg cells can prevent liver injury in AMPKα1-KO mice. In addition, Treg cell-specific AMPKα1-KO mice display histological features similar to those associated with autoimmune liver disease, greater production of autoantibodies, and hyperactivation of CD4
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Registered trials
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.