Transforming growth factor-Β and kidney dysfunction

Jingfei Cheng, Joseph P. Grande

Research output: Contribution to journalReview articlepeer-review

4 Scopus citations


In addition to their critical role in embryogenesis of the kidney, members of the transforming growth factor (TGF)-Β superfamily direct a number of pathways important in the maintenance of homeostasis in the differentiated kidney. TGF-Β family members also play an important role in cell-cycle regulation. Through induction of cyclin-dependent kinase inhibitors, TGF-Β promotes a hypertrophic response of renal tubular epithelial cells and glomerular mesangial cells. This TGF-Β driven hypertrophic response, which occurs in diabetic nephropathy, may have deleterious effects on the kidney. In contrast, many human cancers are associated with loss of the growth inhibitory effects of TGF-Β. TGF-Β may promote or inhibit inflammation, an outcome which appears to depend on the cell type(s) involved and on potential interactions with other signaling pathways that regulate inflammatory responses. In recent studies, TGF-Β has been implicated as a key mediator of the epithelial to mesenchymal transition, a process through which epithelial cells acquire characteristics of myofibroblasts which synthesize and deposit extracellular matrix macromolecules and lead to the development of fibrosis, a characteristic feature of chronic renal disease irrespective of etiology. In this brief overview, we highlight recent advances in our understanding of TGF-Β signaling that contribute to the development and progression of chronic renal disease.

Original languageEnglish (US)
Pages (from-to)182-192
Number of pages11
JournalJournal of Organ Dysfunction
Issue number3
StatePublished - 2009


  • Cell cycle
  • Epithelial to mesenchymal transition
  • Extracellular matrix accumulation
  • Progressive renal disease
  • Signaling, transforming growth factor-Β

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Critical Care
  • Critical Care and Intensive Care Medicine


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