ArticlePloS one2016
Thrombospondin 1 Deficiency Ameliorates the Development of Adriamycin-Induced Proteinuric Kidney Disease.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- The importance of identifying new and putative target antigens associated with membranous nephropathy: evidence from a Sardinian cohort.Clinical kidney journal · 2025Article
- Relationship between circulating thrombospondin-1 messenger ribonucleic acid and microribonucleic acid-194 levels in Chinese patients with type 2 diabetic kidney disease: The outcomes of a case-control study.Journal of diabetes investigation · 2024Article
- Investigating the anti-inflammatory effects of icariin: A combined meta-analysis and machine learning study.Heliyon · 2024Article
- Cell surface GRP78 regulates TGFβ1-mediated profibrotic responsesFrontiers in pharmacology · 2023Article
- Paricalcitol Improves the Angiopoietin/Tie-2 and VEGF/VEGFR2 Signaling Pathways in Adriamycin-Induced Nephropathy.Nutrients · 2022Article
- Signaling pathways of chronic kidney diseases, implications for therapeutics.Signal transduction and targeted therapy · 2022Review
- Induction of Accelerated Aging in a Mouse Model.Cells · 2022Review
- Spatially Resolved Transcriptomes of Mammalian Kidneys Illustrate the Molecular Complexity and Interactions of Functional Nephron Segments.Frontiers in medicine · 2022Article
- Immunomodulatory Role of the Extracellular Matrix Within the Liver Disease Microenvironment.Frontiers in immunology · 2020Review
- Recent Progress on Lipid Intake and Chronic Kidney Disease.BioMed research international · 2020Review
- The role of CD47 in pathogenesis and treatment of renal ischemia reperfusion injury.Pediatric nephrology (Berlin, Germany) · 2019Review
- Kidney disease models: tools to identify mechanisms and potential therapeutic targets.Zoological research · 2018Review
- CD36 in chronic kidney disease: novel insights and therapeutic opportunities.Nature reviews. Nephrology · 2017Review
- Latexin Inactivation Enhances Survival and Long-Term Engraftment of Hematopoietic Stem Cells and Expands the Entire Hematopoietic System in Mice.Stem cell reports · 2017Article
- Role of thrombospondin 1 in liver diseases.Hepatology research : the official journal of the Japan Society of Hepatology · 2017Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Accumulating evidence suggests that thrombospondin 1 (TSP1) is an important player in diabetic nephropathy. However, the role of TSP1 in podocyte injury and the development of non-diabetic proteinuric kidney disease is largely unknown. In the current study, by using a well-established podocyte injury model (adriamycin-induced nephropathy mouse model), we examined the contribution of TSP1 to the development of proteinuric kidney disease. We found that TSP1 was up-regulated in the glomeruli, notably in podocytes, in adriamycin injected mice before the onset of proteinuria. ADR treatment also stimulated TSP1 expression in cultured human podocytes in vitro. Moreover, increased TSP1 mediated ADR-induced podocyte apoptosis and actin cytoskeleton disorganization. This TSP1's effect was through a CD36-dependent mechanism and involved in the stimulation of p38MAPK pathway. Importantly, in vivo data demonstrated that TSP1 deficiency protected mice from ADR induced podocyte loss and foot process effacement. ADR induced proteinuria, glomerulosclerosis, renal macrophage infiltration and inflammation was also attenuated in TSP1 deficient mice. Taken together, these studies provide new evidence that TSP1 contributes to the development of non-diabetic proteinuric kidney disease by stimulating podocyte injury and the progression of renal inflammation.
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