ArticleDiabetologia2013
Caveolin-1 deficiency protects against mesangial matrix expansion in a mouse model of type 1 diabetic nephropathy.
Article in Diabetologia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Organelle Crosstalk in Renal Cells: Insights from Cell Biology and Implications for AKI-to-CKD Transition.International journal of molecular sciences · 2026Review
- miR-299a-5p is a mediator of fibrosis in diabetic kidney disease by regulating follistatin and cripto-1.Communications biology · 2025Article
- Endoplasmic reticulum-mediated organelle crosstalk in kidney disease.Nature reviews. Nephrology · 2025Review
- Crosstalk among podocytes, glomerular endothelial cells and mesangial cells in diabetic kidney disease: an updated review.Cell communication and signaling : CCS · 2024Review
- Diabetic Nephropathy and Gaseous Modulators.Antioxidants (Basel, Switzerland) · 2023Review
- Neuronal regeneration after injury: a new perspective on gene therapy.Frontiers in neuroscience · 2023Article
- Procyanidin B2 suppresses hyperglycemia-induced renal mesangial cell dysfunction by modulating CAV-1-dependent signaling.Experimental and therapeutic medicine · 2022Article
- MRTF: Basic Biology and Role in Kidney Disease.International journal of molecular sciences · 2021Review
- Injury-induced Cavl-expressing cells at lesion rostral side play major roles in spinal cord regeneration.Open biology · 2021Article
- miR299a-5p promotes renal fibrosis by suppressing the antifibrotic actions of follistatin.Scientific reports · 2021Article
- Caveolin-1 Regulates Cellular Metabolism: A Potential Therapeutic Target in Kidney Disease.Frontiers in pharmacology · 2021Review
- Modulation of proteomic and inflammatory signals by Bradykinin in podocytes.Journal of advanced research · 2020Article
- Role of Caveolin-1 in Diabetes and Its Complications.Oxidative medicine and cellular longevity · 2020Review
- Caveolin-1 regulation of Sp1 controls production of the antifibrotic protein follistatin in kidney mesangial cells.Cell communication and signaling : CCS · 2019Article
- Article
- Caveolin-1 in the Pathogenesis of Diabetic Nephropathy: Potential Therapeutic Target?Current diabetes reports · 2017Review
- Loss of Epithelial Membrane Protein 2 Aggravates Podocyte Injury via Upregulation of Caveolin-1.Journal of the American Society of Nephrology : JASN · 2016Article
- Pigment epithelium-derived factor inhibits caveolin-induced interleukin-8 gene expression and proliferation of human prostate cancer cells.Oncology letters · 2015Article
- Interaction among Caveolin-1 genotypes (rs3807987/rs7804372), H. pylori infection, and risk of gastric cancer in a Chinese population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
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7 authors.
Funding
Abstract
aims/hypothesisGlomerular matrix protein accumulation, mediated largely by resident mesangial cells (MCs), is central to the pathogenesis of diabetic nephropathy. We previously showed that caveolin (CAV)-1/caveolae mediate matrix upregulation by MCs in response to high glucose and TGFβ, two important pathogenic mediators of diabetic glomerular sclerosis. Here, we evaluated the in vivo role of CAV-1/caveolae in the development of diabetic nephropathy.
methodsDiabetes was induced in Cav1-knockout (KO) mice and their wild-type (WT) counterparts by streptozotocin injection. After 10 months, kidneys were evaluated for the development of nephropathy, including glomerular sclerosis and upregulation of matrix proteins. Parallel experiments assessing glucose-induced matrix upregulation were carried out in MCs isolated from KO mice.
resultsKO diabetic mice developed hyperglycaemia and renal hypertrophy, but were protected from developing albuminuria and glomerular sclerosis compared with WT mice. KO mice were significantly protected from the upregulation of glomerular collagen I, fibronectin, connective tissue growth factor (CTGF) and TGFβ. In vitro, glucose induced collagen I A1 promoter activation and collagen I, fibronectin and CTGF protein upregulation in WT but not KO MCs. Re-expression of Cav1 in KO cells restored this response. CONCLUSIONS/
interpretationCav1 deletion rendered significant protection from glomerular matrix accumulation and albuminuria in a mouse model of type 1 diabetes. These studies provide a foundation for the development of renal-targeted interference with CAV-1/caveolae as a novel approach to the treatment of diabetic nephropathy.
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