ArticleBMC biology2017
PPARα is essential for retinal lipid metabolism and neuronal survival.
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Article in BMC biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 80 citations in OpenAlex.
- PGC-1α and PPARs cooperatively mediate photoreceptor neuroprotection in rd1 mouse inherited retinal degeneration.Cell death & disease · 2026Article
- Chd7 regulates lipid metabolism and swim bladder inflation in zebrafish.Journal of lipid research · 2026Article
- Polyunsaturated fatty acid metabolism in the retinal pigment epithelium and its association with outer retinal disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Predifferentiation Neurotoxicity of GenX Exposure on hiPSC-Derived Cortical Neurons.Environmental science & technology · 2026Article
- Peroxisome Proliferator-Activated Receptor α Deficiency Induces Vascular Pathologies through Endothelial Senescence in Diabetic Retinopathy.The American journal of pathology · 2026Article
- Identification and validation of a novel ferroptosis-related gene signature associated with inherited retinal degeneration in Rd10 mice.Scientific reports · 2026Article
- Long-acting fenofibrate-loaded microparticles for treating retinal disorders.International journal of pharmaceutics · 2026Article
- Sustained release of a novel non-fibrate PPARα agonist from microparticles for neuroprotection in murine models of age-related macular degeneration.Journal of controlled release : official journal of the Controlled Release Society · 2025Article
- Consensus molecular subtyping of colorectal carcinoma brain metastases reveals a metabolic signature associated with poor patient survival.Molecular oncology · 2025Article
- Systemic regulation of retinal medium-chain fatty acid oxidation repletes TCA cycle flux in oxygen-induced retinopathy.Communications biology · 2025Article
- PPARα deficiency exacerbates retinal pathological changes and dysfunction in high-fat diet mice.International journal of ophthalmology · 2025Article
- Stimulation of Thyroid Hormone Signaling Induces Stress Responses in Mouse Retina.Advances in experimental medicine and biology · 2025Article
- Aryl hydrocarbon receptor (AhR)-mediated immune responses to degeneration of the retinal pigment epithelium.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- Design and Assessment of First-Generation Heterobifunctional PPARα/STING Modulators.ACS medicinal chemistry letters · 2024Article
- Clinical exome analysis and targeted gene repair of the c.1354dupT variant in iPSC lines from patients with PROM1-related retinopathies exhibiting diverse phenotypes.Stem cell research & therapy · 2024Article
- Exploring mitochondrial metabolism of wild-type and diabetic mice skin explants using the Seahorse technology.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
- Hyperbaric oxygen therapy suppresses hypoxia and reoxygenation injury to retinal pigment epithelial cells through activating peroxisome proliferator activator receptor-alpha signalling.Journal of cellular and molecular medicine · 2023Article
- Design, Synthesis, and Structure-Activity Relationships of Biaryl Anilines as Subtype-Selective PPAR-alpha Agonists.ACS medicinal chemistry letters · 2023Article
- Peroxisome proliferator-activated receptor-α (PPARα) regulates wound healing and mitochondrial metabolism in the cornea.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Deficits in mitochondrial TCA cycle and OXPHOS precede rod photoreceptor degeneration during chronic HIF activation.Molecular neurodegeneration · 2023Article
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Authors and funding
17 authors at 5 institutions in 1 country.
Elizabeth A PearsallDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Rui ChengDepartment of Physiology, University of Oklahoma Health Sciences Center, 941 Stanton L. Young Blvd., BSEB 328B, Oklahoma City, OK, 73104, USA.
Kelu ZhouDepartment of Physiology, University of Oklahoma Health Sciences Center, 941 Stanton L. Young Blvd., BSEB 328B, Oklahoma City, OK, 73104, USA.
Yusuke TakahashiDepartment of Physiology, University of Oklahoma Health Sciences Center, 941 Stanton L. Young Blvd., BSEB 328B, Oklahoma City, OK, 73104, USA.
H Greg MatlockDepartment of Physiology, University of Oklahoma Health Sciences Center, 941 Stanton L. Young Blvd., BSEB 328B, Oklahoma City, OK, 73104, USA.
Shraddha S VadvalkarAging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Younghwa ShinDepartment of Physiology, University of Oklahoma Health Sciences Center, 941 Stanton L. Young Blvd., BSEB 328B, Oklahoma City, OK, 73104, USA.
Thomas W FredrickDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Marin L GantnerThe Lowy Medical Research Institute, La Jolla, CA, 92037, USA.
Steven MengDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Zhongjie FuDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Yan GongDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Michael KinterAging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Kenneth M HumphriesAging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Luke I SzwedaAging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Lois E H SmithDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Jian-Xing MaDepartment of Physiology, University of Oklahoma Health Sciences Center, 941 Stanton L. Young Blvd., BSEB 328B, Oklahoma City, OK, 73104, USA. jian-xing-ma@ouhsc.edu.
University of Oklahoma Health Sciences Center · USOklahoma Medical Research Foundation · USHarvard University · USBoston Children's Hospital · USThe Lowy Medical Research Institute · US
Funding
SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI FAGIOLINI, MICHELA · 1985 to 2015
$26.2MTUMOR RESISTANCE MECHANISMS TO ANTI-VEGF THERAPY IN PROSTATE CANCER (Sukyung Woo)P20GM103639 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI DHANASEKARAN, DANNY N. · 2012 to 2022
$21.3MTargeted DNA Methylation and Mitochondrial Heteroplasmy CoreP30AG050911 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI William Edmund Sonntag · 2015 to 2026
$13.9MDietary control of angiogenesis in retinopathy modelsR01EY017017 · NEI · BOSTON CHILDREN'S HOSPITAL · PI Zhongjie Fu, Lois Smith · 2006 to 2026
$11.8MProject 5 VEGF Signaling in PhotoreceptorsP20GM104934 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI HAYS, FRANKLIN ALAN · 2012 to 2016
$10.8MP30-CENTER CORE GRANT FOR VISION RESEARCHP30EY021725 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Michelle C Callegan, MICHAEL H ELLIOTT · 2011 to 2026
$10.5MNovel therapies to inhibit Diabetic RetinopathyR24EY024864 · NEI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KERN, TIMOTHY S · 2015 to 2019
$8.1MTHE ROLE OF MICROVASCULAR CELLS IN NEOVASCULARIZATIONR01EY005318 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI D'AMORE, PATRICIA ANN · 1985 to 2015
$6.4MA new pathogenic mechanism for diabetic retinopathyR01EY019309 · NEI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Jian-Xing Jay Ma · 2009 to 2026
$6.1MSTUDIES OF RPE65R01EY012231 · NEI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, JIAN-XING, MOISEYEV, GENNADIY · 1998 to 2021
$5.7MPilot Project ProgramP30GM122744 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI LE, YUN ZHENG · 2017 to 2021
$5.5MMouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI POMEROY, SCOTT LOREN · 2016 to 2020
$5.2MEuropean Commission 305485 PREVENT-ROPJDRF 2-SRA-2014-147-Q-RJuvenile Diabetes Research Foundation International 3-PDF-2014-107-A-NNational Eye Institute EY018659National Eye Institute EY019309National Eye Institute EY021725National Heart, Lung, and Blood Institute HL125625National Institutes of Health GM103639National Institutes of Health GM104934National Institutes of Health HD18655National Institutes of Health P20GM104934NEI NIH HHS P30 EY021725NEI NIH HHS R01 EY005318NEI NIH HHS R01 EY012231NEI NIH HHS R01 EY017017NEI NIH HHS R01 EY018659NEI NIH HHS R01 EY019309NEI NIH HHS R24 EY024864NHLBI NIH HHS R01 HL125625NIA NIH HHS P30 AG050911NICHD NIH HHS P30 HD018655NICHD NIH HHS U54 HD090255NIGMS NIH HHS P20 GM103639NIGMS NIH HHS P20 GM104934NIGMS NIH HHS P30 GM122744
Abstract
backgroundPeroxisome proliferator activated receptor-alpha (PPARα) is a ubiquitously expressed nuclear receptor. The role of endogenous PPARα in retinal neuronal homeostasis is unknown. Retinal photoreceptors are the highest energy-consuming cells in the body, requiring abundant energy substrates. PPARα is a known regulator of lipid metabolism, and we hypothesized that it may regulate lipid use for oxidative phosphorylation in energetically demanding retinal neurons.
resultsWe found that endogenous PPARα is essential for the maintenance and survival of retinal neurons, with Pparα
conclusionWe identify an endogenous role for PPARα in retinal neuronal survival and lipid metabolism, and furthermore underscore the importance of fatty acid oxidation in photoreceptor survival. We also suggest PPARα as a putative therapeutic target for age-related macular degeneration, which may be due in part to decreased mitochondrial efficiency and subsequent energetic deficits.
Indexed as
Lipid MetabolismAnimalsFatty AcidsMiceMice, Inbred C57BLOxidation-ReductionPPAR alphaRatsRats, Sprague-DawleyRetinaRetinal NeuronsFatty AcidsPPAR alphaAge-related macular degenerationFatty acid oxidationLipidsMitochondriaNeurodegenerationRetinaRetinal energy metabolism
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