ArticleThe Journal of biological chemistry2016
Genetic Ablation of Calcium-independent Phospholipase A2γ Induces Glomerular Injury in Mice.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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
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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Mitochondrial abnormalities in nondiabetic and nonhypertensive glomerular diseases: a comprehensive review.Molecular and cellular biochemistry · 2026Review
- Chloroplast biogenesis involves spatial coordination of nuclear and organellar gene expression in Chlamydomonas.Plant physiology · 2024Article
- Deletion of IRE1α in podocytes exacerbates diabetic nephropathy in mice.Scientific reports · 2024Article
- Genetic deletion of calcium-independent phospholipase A2γ protects mice from diabetic nephropathy.PloS one · 2024Article
- Soluble Klotho protects against glomerular injury through regulation of ER stress response.Communications biology · 2023Article
- Analysis of gene expression and use of connectivity mapping to identify drugs for treatment of human glomerulopathies.Frontiers in medicine · 2023Article
- Review
- The IRE1α pathway in glomerular diseases: The unfolded protein response and beyond.Frontiers in molecular medicine · 2022Review
- Antioxidant Synergy of Mitochondrial Phospholipase PNPLA8/iPLA2γ with Fatty Acid-Conducting SLC25 Gene Family Transporters.Antioxidants (Basel, Switzerland) · 2021Review
- Urinary ERdj3 and mesencephalic astrocyte-derived neutrophic factor identify endoplasmic reticulum stress in glomerular disease.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Regulation of Autophagy Progress via Lysosomal Depletion by Fluvastatin Nanoparticle Treatment in Breast Cancer Cells.ACS omega · 2020Article
- Photosystem Biogenesis Is Localized to the Translation Zone in the Chloroplast of Chlamydomonas.The Plant cell · 2019Article
- Genetic Ablation of Calcium-independent Phospholipase AScientific reports · 2019Article
- Ste20-like kinase, SLK, a novel mediator of podocyte integrity.American journal of physiology. Renal physiology · 2018Article
- Cytoprotective activity of mitochondrial uncoupling protein-2 in lung and spleen.FEBS open bio · 2018Article
- Endoplasmic reticulum stress, the unfolded protein response and autophagy in kidney diseases.Nature reviews. Nephrology · 2017Review
- Deletion of inositol-requiring enzyme-1α in podocytes disrupts glomerular capillary integrity and autophagy.Molecular biology of the cell · 2017Article
- Regulation of Ste20-like kinase, SLK, activity: Dimerization and activation segment phosphorylation.PloS one · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Glomerular visceral epithelial cells (podocytes) play a critical role in the maintenance of glomerular permselectivity. Podocyte injury, manifesting as proteinuria, is the cause of many glomerular diseases. We reported previously that calcium-independent phospholipase A2γ (iPLA2γ) is cytoprotective against complement-mediated glomerular epithelial cell injury. Studies in iPLA2γ KO mice have demonstrated an important role for iPLA2γ in mitochondrial lipid turnover, membrane structure, and metabolism. The aim of the present study was to employ iPLA2γ KO mice to better understand the role of iPLA2γ in normal glomerular and podocyte function as well as in glomerular injury. We show that deletion of iPLA2γ did not cause detectable albuminuria; however, it resulted in mitochondrial structural abnormalities and enhanced autophagy in podocytes as well as loss of podocytes in aging KO mice. Moreover, after induction of anti-glomerular basement membrane nephritis in young mice, iPLA2γ KO mice exhibited significantly increased levels of albuminuria, podocyte injury, and loss of podocytes compared with wild type. Thus, iPLA2γ has a protective functional role in the normal glomerulus and in glomerulonephritis. Understanding the role of iPLA2γ in glomerular pathophysiology provides opportunities for the development of novel therapeutic approaches to glomerular injury and proteinuria.
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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.