From acute injury to chronic disease: pathophysiological hypothesis of an epithelial/mesenchymal crosstalk alteration in CKD | Zendy

Marco Prunotto | Zendy; David C. Budd | Zendy; Matthias Meier | Zendy; Ivan Formentini | Zendy; Guido Hartmann | Zendy; Silvia Pomposiello | Zendy; Solange Moll | Zendy

Open Access

From acute injury to chronic disease: pathophysiological hypothesis of an epithelial/mesenchymal crosstalk alteration in CKD

Author(s) -

Marco Prunotto,

David C. Budd,

Matthias Meier,

Ivan Formentini,

Guido Hartmann,

Silvia Pomposiello,

Solange Moll

Publication year - 2012

Publication title -

nephrology dialysis transplantation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.654

H-Index - 168

eISSN - 1460-2385

pISSN - 0931-0509

DOI - 10.1093/ndt/gfs283

Subject(s) - medicine , kidney disease , mesenchymal stem cell , pathophysiology , crosstalk , fibrosis , acute kidney injury , pathology , kidney , bioinformatics , biology , physics , optics

Observational clinical studies link acute kidney injury to chronic kidney disease (CKD) progression. The pathophysiological mechanisms that underlie this process are currently unknown but recently published papers suggest that tubular epithelial cells and interstitial mesenchymal cells emerge as a single unit, and their integrity alteration as a whole might lead to renal fibrosis and CKD. The present article reviews the biological findings supporting the hypothesis of an altered epithelial/mesenchymal crosstalk in fibrosis development and progression toward CKD.

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