ArticlePloS one2012
Mild electrical stimulation and heat shock ameliorates progressive proteinuria and renal inflammation in mouse model of Alport syndrome.
Article in PloS one, 2012. 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.
- Activation of heat shock response to treat obese subjects with type 2 diabetes: a prospective, frequency-escalating, randomized, open-label, triple-arm trial.Scientific reports · 2016Trial
- Novel Keap1-Nrf2 Protein-Protein Interaction Inhibitor UBE-1099 Ameliorates Progressive Phenotype in Alport Syndrome Mouse Model.Kidney360 · 2022Article
- A novel model of nephrotic syndrome results from a point mutation in Lama5 and is modified by genetic background.Kidney international · 2022Article
- The role of discoidin domain receptor 2 in the renal dysfunction of alport syndrome mouse model.Renal failure · 2021Article
- Mild electrical stimulation with heat shock attenuates renal pathology in adriamycin-induced nephrotic syndrome mouse model.Scientific reports · 2020Article
- Article
- Increased Subfoveal Choroidal Thickness and Retinal Structure Changes on Optical Coherence Tomography in Pediatric Alport Syndrome Patients.Journal of ophthalmology · 2019Article
- Long-term treatment with EGFR inhibitor erlotinib attenuates renal inflammatory cytokines but not nephropathy in Alport syndrome mouse model.Clinical and experimental nephrology · 2017Article
- Bromide supplementation exacerbated the renal dysfunction, injury and fibrosis in a mouse model of Alport syndrome.PloS one · 2017Article
- Podocyte p53 Limits the Severity of Experimental Alport Syndrome.Journal of the American Society of Nephrology : JASN · 2016Article
- Induction of Heat Shock Proteins in the Therapy of Type 2 Diabetes and Metabolic Syndrome.EBioMedicine · 2014Article
- Article
- Mild electrical stimulation at 0.1-ms pulse width induces p53 protein phosphorylation and G2 arrest in human epithelial cells.The Journal of biological chemistry · 2013Article
- p38/AP-1 pathway in lipopolysaccharide-induced inflammatory responses is negatively modulated by electrical stimulation.Mediators of inflammation · 2013Article
- Alport Syndrome Classification and Management.Kidney medicineReview
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alport syndrome is a hereditary glomerulopathy with proteinuria and nephritis caused by defects in genes encoding type IV collagen in the glomerular basement membrane. All male and most female patients develop end-stage renal disease. Effective treatment to stop or decelerate the progression of proteinuria and nephritis is still under investigation. Here we showed that combination treatment of mild electrical stress (MES) and heat stress (HS) ameliorated progressive proteinuria and renal injury in mouse model of Alport syndrome. The expressions of kidney injury marker neutrophil gelatinase-associated lipocalin and pro-inflammatory cytokines interleukin-6, tumor necrosis factor-α and interleukin-1β were suppressed by MES+HS treatment. The anti-proteinuric effect of MES+HS treatment is mediated by podocytic activation of phosphatidylinositol 3-OH kinase (PI3K)-Akt and heat shock protein 72 (Hsp72)-dependent pathways in vitro and in vivo. The anti-inflammatory effect of MES+HS was mediated by glomerular activation of c-jun NH(2)-terminal kinase 1/2 (JNK1/2) and p38-dependent pathways ex vivo. Collectively, our studies show that combination treatment of MES and HS confers anti-proteinuric and anti-inflammatory effects on Alport mice likely through the activation of multiple signaling pathways including PI3K-Akt, Hsp72, JNK1/2, and p38 pathways, providing a novel candidate therapeutic strategy to decelerate the progression of patho-phenotypes in Alport syndrome.
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