ArticleNature communications2022
REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation.
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 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- REDD1 Silencing Aggravates Aortic Dissection and Promotes VSMC Apoptosis with Autophagy-Related Changes.Biomedicines · 2026Article
- Chromium(III) Beyond Insulin: A Mechanistic Roadmap Across the Energy-Redox-Inflammation Triad in Obesity and Cardiometabolic Disease.Biological trace element research · 2026Review
- Hippocampal REDD1 inhibition is critical for alleviating depressive-like behaviors.Acta pharmacologica Sinica · 2026Article
- Sustained intravitreal delivery of carnosic acid by RADA16 peptide hydrogel protects the retina in acute ocular hypertension.Scientific reports · 2026Article
- Prostaglandin E2 alleviates acetaminophen-induced liver injury through DDIT4-enhanced autophagy regulated by circLima1/miR-486.Scientific reports · 2026Article
- Inhibition of GPR75 Alleviates Lipid Metabolism by Activating the AMPK-SIRT1 Signaling Pathway In Vitro and In Vivo.Molecular biotechnology · 2026Article
- The REDD1-NF-κB-miRNAs-eNOS/SIRT1 axis mediates obesity-induced endothelial cell senescence and hypertension.Nature communications · 2026Article
- Adipocyte-specific NR5A2 deficiency ameliorates diet-induced metabolic syndrome by suppressing adipose tissue inflammation.Scientific reports · 2026Article
- Siglec-E deletion alters AT macrophages phenotypes, induces an inflammatory response, and adipogenesis during diet-induced obesity.International immunopharmacology · 2026Article
- Obesity-cancer axis crosstalk: Molecular insights and therapeutic approaches.Acta pharmaceutica Sinica. B · 2025Review
- Podocyte-Specific Expression of the Stress Response Protein REDD1 Is Necessary for Diabetes-Induced Podocytopenia.Diabetes · 2025Article
- REDD1 expression in podocytes facilitates renal inflammation and pyroptosis in streptozotocin-induced diabetic nephropathy.Cell death & disease · 2025Article
- Siglec-E augments adipose tissue inflammation by modulating TRAF3 signaling and monocytic myeloid-derived suppressor cells during obesity.Frontiers in immunology · 2025Article
- Review
- Dietary pyruvate targets cytosolic phospholipase A2 to mitigate inflammation and obesity in mice.Protein & cell · 2024Article
- REDD1 Deletion Suppresses NF-κB Signaling in Cardiomyocytes and Prevents Deficits in Cardiac Function in Diabetic Mice.International journal of molecular sciences · 2024Article
- Alleviation of preeclampsia-like symptoms through PlGF and eNOS regulation by hypoxia- and NF-κB-responsive miR-214-3p deletion.Experimental & molecular medicine · 2024Article
- The stress-responsive protein REDD1 and its pathophysiological functions.Experimental & molecular medicine · 2023Review
- Leaf Extract ofNutrients · 2023Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulated in development and DNA damage response 1 (REDD1) expression is upregulated in response to metabolic imbalance and obesity. However, its role in obesity-associated complications is unclear. Here, we demonstrate that the REDD1-NF-κB axis is crucial for metabolic inflammation and dysregulation. Mice lacking Redd1 in the whole body or adipocytes exhibited restrained diet-induced obesity, inflammation, insulin resistance, and hepatic steatosis. Myeloid Redd1-deficient mice showed similar results, without restrained obesity and hepatic steatosis. Redd1-deficient adipose-derived stem cells lost their potential to differentiate into adipocytes; however, REDD1 overexpression stimulated preadipocyte differentiation and proinflammatory cytokine expression through atypical IKK-independent NF-κB activation by sequestering IκBα from the NF-κB/IκBα complex. REDD1 with mutated Lys
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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.