More than 10% of the population are suffering chronic kidney disease (CKD), result from multiple etiology including diabetes, hypertension, immunological disease, kidney stone, and acute kidney injury-related chronic damage. Renal fibrosis would be the final pathological change among all types of chronic ...
More than 10% of the population are suffering chronic kidney disease (CKD), result from multiple etiology including diabetes, hypertension, immunological disease, kidney stone, and acute kidney injury-related chronic damage. Renal fibrosis would be the final pathological change among all types of chronic kidney disease, but the molecular mechanism might not be the same. Short of well-accepted anti-fibrosis medicine and the new-onset end-stage renal disease (ESRD) cases are growing rapidly all around the world. Therefore, the discovery of disease targets would be the key research focus for researchers in nephrology and pharmacology. Potent candidate small molecule compounds with anti-fibrosis characteristics will provide novel avenues for therapeutic intervention.
This Research Topic focuses on the pathogenesis and therapeutic target identification of renal interstitial fibrosis, as well as therapeutic agent candidates for well-recognized targets. We welcome submissions of Original Research and Reviews articles on the subtopics below, especially studies with function validation, and in vitro or in vivo data.
• Hyperglycemia induced epithelial-mesenchymal transition
• Primary or secondary oxalate nephropathy
• Essential hypertension-related interstitial fibrosis
• Renal tubular injury result from endotoxins and inflammation
Keywords:
Interstitial Fibrosis, Tubular Cell, Small molecular compounds, Epithelial-mesenchymal transition
Important Note:
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