ArticleNature medicine2010
Rtp801, a suppressor of mTOR signaling, is an essential mediator of cigarette smoke-induced pulmonary injury and emphysema.
Article in Nature medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.
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Who cites it
131 citing papers in PubMed, 1 synthesis or guideline pooled it, 238 citations in OpenAlex.
- The interplay between oxidative stress and autophagy in chronic obstructive pulmonary disease.Frontiers in physiology · 2022Pooled it
- A common germline 3' UTR variant controls DDIT4 translation efficiency and stress responses in cancer cells.iScience · 2026Article
- Stress granule dynamics orchestrate colitis-to-cancer transition via TOM1-mediated disassembly and driven oncogenesis in response to inflammatory oxidative stress.Redox biology · 2026Article
- Smoke Condensate-Induced Vascular Senescence and SASP Are Attenuated by Dual mTORC1/2 Inhibition with Rapalink-1.International journal of molecular sciences · 2026Article
- The mTOR Inhibitor Rapamycin Attenuates Ozone-Induced Airway Inflammation and Emphysema In Mice.Journal of inflammation research · 2026Article
- The dual role of mTOR signaling in lung development and adult lung diseases.Cell & bioscience · 2025Review
- Short-Term and Long-Term Effects of Electronic Cigarettes on Mouse Lungs Following Nose-Only Exposures.Chemical research in toxicology · 2025Article
- REDD1 mediates HDM-induced nuclear-cytoplasmic translocation and release of IL-33 in airway epithelial cells by downregulating Nrf2.Respiratory research · 2025Article
- YTHDF2 promotes anaplastic thyroid cancer progression by activating the DDIT4/AKT/mTOR signaling pathway.Biology direct · 2024Article
- Review
- Neuroinflammation and Brain Health Risks in Veterans Exposed to Burn Pit Toxins.International journal of molecular sciences · 2024Review
- REDD1 Deletion Suppresses NF-κB Signaling in Cardiomyocytes and Prevents Deficits in Cardiac Function in Diabetic Mice.International journal of molecular sciences · 2024Article
- Unraveling the Impact ofLife (Basel, Switzerland) · 2024Article
- Targeting accelerated pulmonary ageing to treat chronic obstructive pulmonary disease-induced neuropathological comorbidities.British journal of pharmacology · 2024Review
- The stress-responsive protein REDD1 and its pathophysiological functions.Experimental & molecular medicine · 2023Review
- 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
- Molecular, cellular and neurological consequences of infection by the neglected human pathogen Nocardia.BMC biology · 2022Article
- REDD1 promotes obesity-induced metabolic dysfunction via atypical NF-κB activation.Nature communications · 2022Article
- Review
- The mMolecular cancer · 2022Article
71 more citing papers are in PubMed but not listed here.
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25 authors at 4 institutions in 1 country.
Funding
Abstract
Rtp801 (also known as Redd1, and encoded by Ddit4), a stress-related protein triggered by adverse environmental conditions, inhibits mammalian target of rapamycin (mTOR) by stabilizing the TSC1-TSC2 inhibitory complex and enhances oxidative stress-dependent cell death. We postulated that Rtp801 acts as a potential amplifying switch in the development of cigarette smoke-induced lung injury, leading to emphysema. Rtp801 mRNA and protein were overexpressed in human emphysematous lungs and in lungs of mice exposed to cigarette smoke. The regulation of Rtp801 expression by cigarette smoke may rely on oxidative stress-dependent activation of the CCAAT response element in its promoter. We also found that Rtp801 was necessary and sufficient for nuclear factor-kappaB (NF-kappaB) activation in cultured cells and, when forcefully expressed in mouse lungs, it promoted NF-kappaB activation, alveolar inflammation, oxidative stress and apoptosis of alveolar septal cells. In contrast, Rtp801 knockout mice were markedly protected against acute cigarette smoke-induced lung injury, partly via increased mTOR signaling, and, when exposed chronically to cigarette smoke, against emphysema. Our data support the notion that Rtp801 may represent a major molecular sensor and mediator of cigarette smoke-induced lung injury.
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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.