ReviewExperimental & molecular medicine2023
The stress-responsive protein REDD1 and its pathophysiological functions.
Review in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
- REDD1 Silencing Aggravates Aortic Dissection and Promotes VSMC Apoptosis with Autophagy-Related Changes.Biomedicines · 2026Article
- NeuronaleNeuro · 2026Article
- Inorganic Nanomaterials can Promote or Inhibit Tumor Metastasis Depending on Tumor Microenvironment Composition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Hippocampal REDD1 inhibition is critical for alleviating depressive-like behaviors.Acta pharmacologica Sinica · 2026Article
- REDD1 deficiency alleviates podocyte PANoptosis and restores autophagy in diabetic kidney disease.Molecular medicine (Cambridge, Mass.) · 2026Article
- Transcriptomic Profiling of Monozygotic Twins with Type 1 Gaucher Disease.Life (Basel, Switzerland) · 2026Article
- A genetic screen for regulators of Drosophila histone H1 binding and chromosome structure in vivo.Genetics · 2026Article
- REDD1/DDIT4 counteracts endoplasmic reticulum stress-induced apoptosis by controlling the expression of death receptor TRAILR2/DR5 in cancer cells.Cell death & disease · 2026Article
- The REDD1-NF-κB-miRNAs-eNOS/SIRT1 axis mediates obesity-induced endothelial cell senescence and hypertension.Nature communications · 2026Article
- Disease modeling of myocilin mutation-dependent normal tension glaucoma: human retinal ganglion cell susceptibility to unfolded protein response and mTOR signaling.Stem cells (Dayton, Ohio) · 2026Article
- Critical Roles and Molecular Mechanisms of Chaperone-Mediated Autophagy in Infections.International journal of molecular sciences · 2026Review
- Decoding Non-Neuronal Mechanisms and Therapeutic Targets in Huntington's Disease Through Integrative Transcriptomics and Machine Learning.Journal of molecular neuroscience : MN · 2026Article
- Article
- Shaping Cell Identity: Global Transcriptome and Pathway Shifts during Mouse Mammary Epithelial Cell Differentiation.Computational and structural biotechnology journal · 2026Article
- Nomilin Rewires mTOR-Driven Immunometabolism via DDIT4 to Restrain Psoriasis.International journal of biological sciences · 2026Article
- METTL14-mediated mEpigenetics · 2025Article
- Adipose-derived mesenchymal stem cell therapy modulates mitochondrial function to attenuate acetaminophen-induced liver injury by DDIT4/PGC-1α axis.Stem cell research & therapy · 2025Article
- Cell Type-Specific mTORC1 Signaling and Translational Control in Synaptic Plasticity and Memory.Journal of neurochemistry · 2025Review
- Hyperglycemia Modulates mTOR Signaling and Myelin Protein Expression in Schwann Cells.International journal of molecular sciences · 2025Article
- Single-cell transcriptomics of neuroinflammation and cerebrovascular endothelial cells in the aged rat hippocampus.iScience · 2025Article
Corrections and comments
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Authors and funding
3 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) is a stress-induced protein that controls various cellular functions, including metabolism, oxidative stress, autophagy, and cell fate, and contributes to the pathogenesis of metabolic and inflammatory disorders, neurodegeneration, and cancer. REDD1 usually exerts deleterious effects, including tumorigenesis, metabolic inflammation, neurodegeneration, and muscle dystrophy; however, it also exhibits protective functions by regulating multiple intrinsic cell activities through either an mTORC1-dependent or -independent mechanism. REDD1 typically regulates mTORC1 signaling, NF-κB activation, and cellular pro-oxidant or antioxidant activity by interacting with 14-3-3 proteins, IκBα, and thioredoxin-interacting protein or 75 kDa glucose-regulated protein, respectively. The diverse functions of REDD1 depend on cell type, cellular context, interaction partners, and cellular localization (e.g., mitochondria, endomembrane, or cytosol). Therefore, comprehensively understanding the molecular mechanisms and biological roles of REDD1 under pathophysiological conditions is of utmost importance. In this review, based on the published literature, we highlight and discuss the molecular mechanisms underlying the REDD1 expression and its actions, biological functions, and pathophysiological roles.
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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.