ArticleThe American journal of pathology2014
Thrombospondin-1 deficiency causes a shift from fibroproliferative to inflammatory kidney disease and delays onset of renal failure.
Article in The American journal of pathology, 2014. 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, 23 citations in OpenAlex.
- Influence of Soluble Guanylate Cyclase on Cardiac, Vascular, and Renal Structure and Function: A Physiopathological Insight.International journal of molecular sciences · 2025Review
- ADAMTS13 attenuates renal fibrosis by suppressing thrombospondin 1 mediated TGF-β1/Smad3 activation.Toxicology and applied pharmacology · 2025Article
- Comparison of the surgical resection and infarct 5/6 nephrectomy rat models of chronic kidney disease.American journal of physiology. Renal physiology · 2022Review
- Thrombospondin 1 Promotes Endoplasmic Reticulum Stress and Apoptosis in HK-2 Cells by Upregulating ATF6-CHOP.Current medical science · 2022Article
- Thrombospondin 1 and Its Diverse Roles as a Regulator of Extracellular Matrix in Fibrotic Disease.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Review
- Astaxanthin ameliorates renal interstitial fibrosis and peritubular capillary rarefaction in unilateral ureteral obstruction.Molecular medicine reports · 2019Article
- Thrombospondin-4 in tissue remodeling.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- Podocyte-Specific Induction of Krüppel-Like Factor 15 Restores Differentiation Markers and Attenuates Kidney Injury in Proteinuric Kidney Disease.Journal of the American Society of Nephrology : JASN · 2018Article
- Thrombospondin-1 regulation of latent TGF-β activation: A therapeutic target for fibrotic disease.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- 3D virtual histology of murine kidneys -high resolution visualization of pathological alterations by micro computed tomography.Scientific reports · 2018Article
- Role of thrombospondin 1 in liver diseases.Hepatology research : the official journal of the Japan Society of Hepatology · 2017Review
- Feature selection and classification of urinary mRNA microarray data by iterative random forest to diagnose renal fibrosis: a two-stage study.Scientific reports · 2017Article
- Fibroblast-Extracellular Matrix Interactions in Tissue Fibrosis.Current pathobiology reports · 2016Article
- Thrombospondin 1 Modulates Monocyte Properties to Suppress Intestinal Mucosal Inflammation.Journal of innate immunity · 2015Article
- Precision renal medicine: a roadmap towards targeted kidney fibrosis therapies.Fibrogenesis & tissue repair · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Thrombospondin-1 (TSP1) is a multifunctional matricellular protein known to promote progression of chronic kidney disease. To gain insight into the underlying mechanisms through which TSP1 accelerates chronic kidney disease, we compared disease progression in Col4a3 knockout (KO) mice, which develop spontaneous kidney failure, with that of Col4a3;Tsp1 double-knockout (DKO) mice. Decline of excretory renal function was significantly delayed in the absence of TSP1. Although Col4a3;Tsp1 DKO mice did progress toward end-stage renal failure, their kidneys exhibited distinct histopathological lesions, compared with creatinine level-matched Col4a3 KO mice. Although kidneys of both Col4a3 KO and Col4a3;Tsp1 DKO mice exhibited a widened tubulointerstitium, predominant lesions in Col4a3 KO kidneys were collagen deposition and fibroblast accumulation, whereas in Col4a3;Tsp1 DKO kidney inflammation was predominant, with less collagen deposition. Altered disease progression correlated with impaired activation of transforming growth factor-β1 (TGF-β1) in vivo and in vitro in the absence of TSP1. In summary, our findings suggest that TSP1 contributes to progression of chronic kidney disease by catalyzing activation of latent TGF-β1, resulting in promotion of a fibroproliferative response over an inflammatory response. Furthermore, the findings suggest that fibroproliferative and inflammatory lesions are independent entities, both of which contribute to decline of renal function.
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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.