ArticleNature metabolism2020
RIPK1 gene variants associate with obesity in humans and can be therapeutically silenced to reduce obesity in mice.
Article in Nature metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers, 1 of them a synthesis that pooled it.
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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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- An integrated single cell and spatial transcriptomic map of human white adipose tissue.Nature communications · 2023Pooled it
- Programmed cell death in metabolic syndrome: From molecular mechanisms to therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- Adipocyte caspase-8 but not RIPK3 promotes adiposity.Cell death discovery · 2026Article
- Hyperlipidemia induces hippocampal inflammation and loss of vascularity and can be rescued by silencing RIPK1.Scientific reports · 2026Article
- Targeting necroptosis: how does exercise protect against metabolic dysfunction-associated fatty liver disease?Frontiers in physiology · 2026Review
- A Global Transcriptomic Analysis Reveals Body Weight-Specific Molecular Responses to Chronic Orange Juice Consumption in Healthy Individuals.Molecular nutrition & food research · 2025Article
- Adipocyte-specific Mlkl knockout mitigates obesity-induced metabolic dysfunction by enhancing mitochondrial functions.Cell death & disease · 2025Article
- Linear ubiquitination prevents lipodystrophy and obesity-associated metabolic syndrome.Science advances · 2025Article
- Placental Gene Expression Associated With Early Childhood Growth Trajectories and Obesity Risk.Obesity (Silver Spring, Md.) · 2025Article
- Pharmacological Evaluation ofCurrent issues in molecular biology · 2025Article
- Variant-to-function approaches for adipose tissue: Insights into cardiometabolic disorders.Cell genomics · 2025Review
- Life-threatening risk factors contribute to the development of diseases with the highest mortality through the induction of regulated necrotic cell death.Cell death & disease · 2025Review
- Reduction of intestinal RIPK1 ameliorates HFD-induced metabolic disorders in female mice.iScience · 2025Article
- Divergent roles of RIPK3 and MLKL in high-fat diet-induced obesity and MAFLD in mice.Life science alliance · 2025Article
- Article
- Mediators of necroptosis: from cell death to metabolic regulation.EMBO molecular medicine · 2024Review
- Targeted Proteomics Reveals Functional Targets for Early Diabetes Susceptibility in Young Adults.Circulation. Genomic and precision medicine · 2024Article
- Polarity protein AF6 functions as a modulator of necroptosis by regulating ubiquitination of RIPK1 in liver diseases.Cell death & disease · 2023Article
- A common human MLKL polymorphism confers resistance to negative regulation by phosphorylation.Nature communications · 2023Article
- A single nuclei atlas of aging human abdominal subcutaneous white adipose tissue.Research square · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
30 authors at 8 institutions in 4 countries.
Funding
Abstract
Obesity is a major public health burden worldwide and is characterized by chronic low-grade inflammation driven by the cooperation of the innate immune system and dysregulated metabolism in adipose tissue and other metabolic organs. Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) is a central regulator of inflammatory cell function that coordinates inflammation, apoptosis and necroptosis in response to inflammatory stimuli. Here we show that genetic polymorphisms near the human RIPK1 locus associate with increased RIPK1 gene expression and obesity. We show that one of these single nucleotide polymorphisms is within a binding site for E4BP4 and increases RIPK1 promoter activity and RIPK1 gene expression in adipose tissue. Therapeutic silencing of RIPK1 in vivo in a mouse model of diet-induced obesity dramatically reduces fat mass, total body weight and improves insulin sensitivity, while simultaneously reducing macrophage and promoting invariant natural killer T cell accumulation in adipose tissue. These findings demonstrate that RIPK1 is genetically associated with obesity, and reducing RIPK1 expression is a potential therapeutic approach to target obesity and related diseases.
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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.