ArticleScientific reports2017
Implication of REDD1 in the activation of inflammatory pathways.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 64 citations in OpenAlex.
- REDD1/DDIT4 counteracts endoplasmic reticulum stress-induced apoptosis by controlling the expression of death receptor TRAILR2/DR5 in cancer cells.Cell death & disease · 2026Article
- Exosomes derived from MSCs exposed to hypoxic and inflammatory environments slow intervertebral disc degeneration by alleviating the senescence of nucleus pulposus cells through epigenetic modifications.Bioactive materials · 2025Article
- Deletion of the stress response protein REDD1 prevents sodium iodate-induced RPE damage and photoreceptor loss.GeroScience · 2025Article
- REDD1 expression in podocytes facilitates renal inflammation and pyroptosis in streptozotocin-induced diabetic nephropathy.Cell death & disease · 2025Article
- REDD1 mediates HDM-induced nuclear-cytoplasmic translocation and release of IL-33 in airway epithelial cells by downregulating Nrf2.Respiratory research · 2025Article
- Targeting the NLRP3 inflammasome in kidney disease: molecular mechanisms, pathogenic roles, and emerging small-molecule therapeutics.Frontiers in immunology · 2025Review
- Genome-wide association study and transcriptomic analysis reveal the crucial role ofFrontiers in immunology · 2025Article
- Review
- REDD1 Deletion Suppresses NF-κB Signaling in Cardiomyocytes and Prevents Deficits in Cardiac Function in Diabetic Mice.International journal of molecular sciences · 2024Article
- The stress-responsive protein REDD1 and its pathophysiological functions.Experimental & molecular medicine · 2023Review
- Small extracellular vesicles-transported lncRNA TDRKH-AS1 derived from AOPPs-treated trophoblasts initiates endothelial cells pyroptosis through PDIA4/DDIT4 axis in preeclampsia.Journal of translational medicine · 2023Article
- PERK/ATF4-dependent expression of the stress response protein REDD1 promotes proinflammatory cytokine expression in the heart of obese mice.American journal of physiology. Endocrinology and metabolism · 2023Article
- REDD1 deletion and treadmill running increase liver hepcidin and gluconeogenic enzymes in male mice.Journal of nutritional science · 2023Article
- REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation.Nature communications · 2022Article
- Mechanisms of cancer cell death induction by paclitaxel: an updated review.Apoptosis : an international journal on programmed cell death · 2022Review
- Nutritional Sensor REDD1 in Cancer and Inflammation: Friend or Foe?International journal of molecular sciences · 2022Review
- Article
- Long Non-coding Antisense RNA DDIT4-AS1 Regulates Meningitic Escherichia coli-Induced Neuroinflammation by Promoting DDIT4 mRNA Stability.Molecular neurobiology · 2022Article
- RTP801/REDD1 Is Involved in Neuroinflammation and Modulates Cognitive Dysfunction in Huntington's Disease.Biomolecules · 2021Article
- TNFα Mediates Inflammation-Induced Effects onCells · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In response to endotoxemia, the organism triggers an inflammatory response, and the visceral adipose tissue represents a major source of proinflammatory cytokines. The regulation of inflammation response in the adipose tissue is thus of crucial importance. We demonstrated that Regulated in development and DNA damage response-1 (REDD1) is involved in inflammation. REDD1 expression was increased in response to lipopolysaccharide (LPS) in bone marrow derived macrophages (BMDM) and in epidydimal adipose tissue. Loss of REDD1 protected the development of inflammation, since the expression of proinflammatory cytokines (TNFα, IL-6, IL-1β) was decreased in adipose tissue of REDD1
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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.