ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2008
Vitamin A depletion causes oxidative stress, mitochondrial dysfunction, and PARP-1-dependent energy deprivation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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The trial behind it
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
48 citing papers in PubMed, 92 citations in OpenAlex.
- Review
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- Differential proteomic profiles between cognitive frail and robust older adults from the MELoR cohort.GeroScience · 2025Article
- Vitamin A retinoic acid contributes to muscle stem cell and mitochondrial function loss in old age.JCI insight · 2025Article
- Vitamin A treatment restores vision failures arising from Leber's hereditary optic neuropathy-linked mtDNA mutation.JCI insight · 2025Article
- UPLC-QqQMS based targeted metabolomics reveal combination impact on metabolism caused by bisphenol AF and fructose combined exposure in male mice.Scientific reports · 2025Article
- Mitochondrial Dysfunction and Atherosclerosis: The Problem and the Search for Its Solution.Biomedicines · 2025Review
- ROS Chronicles in HIV Infection: Genesis of Oxidative Stress, Associated Pathologies, and Therapeutic Strategies.Current issues in molecular biology · 2024Review
- Uncommon opsin's retinal isomer is involved in mammalian sperm thermotaxis.Scientific reports · 2024Article
- NLRX1 Inhibits LPS-Induced Microglial Death via Inducing p62-Dependent HO-1 Expression, Inhibiting MLKL and Activating PARP-1.Antioxidants (Basel, Switzerland) · 2024Article
- Microneedles: A novel clinical technology for evaluating skin characteristics.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Article
- Targeting mitochondria with antioxidant nutrients for the prevention and treatment of postweaning diarrhea in piglets.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023Review
- Assessing Metabolic Differences Associated with Exposure to Polybrominated Biphenyl and Polychlorinated Biphenyls in the Michigan PBB Registry.Environmental health perspectives · 2023Article
- Retinoic Acid Prevents α-Synuclein Preformed Fibrils-Induced Toxicity via Inhibiting STAT1-PARP1 Signaling.Molecular neurobiology · 2023Article
- Quantum chemistry rules retinoid biology.Communications biology · 2023Review
- Targeting the Retinoic Acid Pathway to Eradicate Cancer Stem Cells.International journal of molecular sciences · 2023Review
- Vitamin A Deficiency Alters the Phototransduction Machinery and Distinct Non-Vision-Specific Pathways in theBiomolecules · 2022Article
- Personalized Medicine in Mitochondrial Health and Disease: Molecular Basis of Therapeutic Approaches Based on Nutritional Supplements and Their Analogs.Molecules (Basel, Switzerland) · 2022Review
- Antagonizing RARγ Drives Necroptosis of Cancer Stem Cells.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
A significant unresolved question is how vitamin A deprivation causes, and why retinoic acid fails to reverse, immunodeficiency. When depleted of vitamin A, T cells undergo programmed cell death (PCD), which is enhanced by the natural competitor of retinol, anhydroretinol. PCD does not happen by apoptosis, despite the occurrence of shared early events, including mitochondrial membrane depolarization, permeability transition pore opening, and cytochrome c release. It also lacks caspase-3 activation, chromatin condensation, and endonuclease-mediated DNA degradation, hallmarks of apoptosis. PCD following vitamin A deprivation exhibits increased production of reactive oxygen species (ROS), drastic reductions in ATP and NAD(+) levels, and activation of poly-(ADP-ribose) polymerase (PARP) -1. These latter steps are causative because neutralizing ROS, imposing hypoxic conditions, or inhibiting PARP-1 by genetic or pharmacologic approaches prevents energy depletion and PCD. The data highlight a novel regulatory role of vitamin A in mitochondrial energy homeostasis.
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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.