ArticleJCI insight2023
Targeting activin receptor-like kinase 7 ameliorates adiposity and associated metabolic disorders.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Review
- GDF3 promotes adipose tissue macrophage-mediated inflammation via altered chromatin accessibility during aging.Nature aging · 2026Article
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- A consensus guide to preclinical indirect calorimetry experiments.Nature metabolism · 2025Review
- Activin Actions in Adipocytes.The Journal of clinical endocrinology and metabolism · 2025Review
- Acute regulation of murine adipose tissue lipolysis and insulin resistance by the TGFβ superfamily protein GDF3.Nature communications · 2025Article
- Recent advances in targeting obesity, with a focus on TGF-β signaling and vagus nerve innervation.Bioelectronic medicine · 2025Review
- Dapagliflozin alleviates high-fat-induced obesity cardiomyopathy by inhibiting ferroptosis.ESC heart failure · 2025Article
- Combined Hyaluronic Acid Nanobioconjugates Impair CD44-Signaling for Effective Treatment Against Obesity: A Review of Comparison with Other Actors.International journal of nanomedicine · 2025Review
- Macrophages: their role in immunity and their relationship with fatty acids in health and disease.Frontiers in immunology · 2025Review
- Paradigm shift in obesity treatment: an extensive review of current pipeline agents.Turkish journal of medical sciences · 2025Review
- Activin E is a transforming growth factor β ligand that signals specifically through activin receptor-like kinase 7.The Biochemical journal · 2024Article
- Human ACVR1C missense variants that correlate with altered body fat distribution produce metabolic alterations of graded severity in knock-in mutant mice.Molecular metabolism · 2024Article
- Targeting the activin receptor 1C on CD4+ T cells for cancer immunotherapy.Oncoimmunology · 2024Article
- Hepatic Activin E mediates liver-adipose inter-organ communication, suppressing adipose lipolysis in response to elevated serum fatty acids.Molecular metabolism · 2023Article
- Activin E-ACVR1C cross talk controls energy storage via suppression of adipose lipolysis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activin receptor-like kinase 7 (ALK7) is a type I receptor in the TGF-β superfamily preferentially expressed in adipose tissue and associated with lipid metabolism. Inactivation of ALK7 signaling in mice results in increased lipolysis and resistance to both genetic and diet-induced obesity. Human genetic studies have recently revealed an association between ALK7 variants and both reduced waist to hip ratios and resistance to development of diabetes. In the present study, treatment with a neutralizing mAb against ALK7 caused a substantial loss of adipose mass and improved glucose intolerance and insulin resistance in both genetic and diet-induced mouse obesity models. The enhanced lipolysis increased fatty acid supply from adipocytes to promote fatty acid oxidation in muscle and oxygen consumption at the whole-body level. The treatment temporarily increased hepatic triglyceride levels, which resolved with long-term Ab treatment. Blocking of ALK7 signals also decreased production of its ligand, growth differentiation factor 3, by downregulating S100A8/A9 release from adipocytes and, subsequently, IL-1β release from adipose tissue macrophages. These findings support the feasibility of potential therapeutics targeting ALK7 as a treatment for obesity and diabetes.
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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.