Tubulointerstitial fibrosis is a chronic and progressive process affecting kidneys during aging and in chronic kidney disease (CKD), regardless of cause. CKD and renal fibrosis affect half of adults above age 70 and 10% of the world's population. Although no targeted therapy yet exists to slow renal fibrosis, a number of important recent advances have clarified the cellular and molecular mechanisms underlying the disease. In this review, I highlight these advances with a focus on cells and pathways that may be amenable to therapeutic targeting. I discuss pathologic changes regulating interstitial myofibroblast activation, including profibrotic and proinflammatory paracrine signals secreted by epithelial cells after either acute or chronic injury. I conclude by highlighting novel therapeutic targets and approaches with particular promise for development of new treatments for patients with fibrotic kidney disease.
Research Article: Journal of Renal Medicine
Research Article: Journal of Renal Medicine
Research Article: Journal of Renal Medicine
Research Article: Journal of Renal Medicine
Review Article: Journal of Renal Medicine
Review Article: Journal of Renal Medicine
Research Article: Journal of Renal Medicine
Research Article: Journal of Renal Medicine
Research Article: Journal of Renal Medicine
Research Article: Journal of Renal Medicine
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Posters & Accepted Abstracts: Journal of Aesthetic & Reconstructive Surgery
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Posters & Accepted Abstracts: Journal of Medical Physics and Applied Sciences
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ScientificTracks Abstracts: Journal of Obesity & Eating Disorders
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Posters & Accepted Abstracts: Journal of Pediatric Care
Posters & Accepted Abstracts: Journal of Obesity & Eating Disorders
Posters & Accepted Abstracts: Journal of Obesity & Eating Disorders
Journal of Renal Medicine received 55 citations as per Google Scholar report