Potential therapeutic effects of natural compounds targeting autophagy to alleviate podocyte injury in glomerular diseases

Podocyte injury is a common cause of proteinuric kidney diseases. Uncontrollable progressive podocyte loss accelerates glomerulosclerosis and increases the risk of end-stage renal disease. To date, owing to the complex pathological mechanism, effective therapies for podocyte injury have been limited...

Full description

Saved in:
Bibliographic Details
Published inBiomedicine & pharmacotherapy Vol. 155; p. 113670
Main Authors Liu, Tongtong, Jin, Qi, Ren, Feihong, Yang, Liping, Mao, Huimin, Ma, Fang, Wang, Yuyang, Li, Ping, Zhan, Yongli
Format Journal Article
LanguageEnglish
Published Elsevier Masson SAS 01.11.2022
Elsevier
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Podocyte injury is a common cause of proteinuric kidney diseases. Uncontrollable progressive podocyte loss accelerates glomerulosclerosis and increases the risk of end-stage renal disease. To date, owing to the complex pathological mechanism, effective therapies for podocyte injury have been limited. Accumulating evidence supports the indispensable role of autophagy in the maintenance of podocyte homeostasis. A variety of natural compounds and their derivatives have been found to regulate autophagy through multiple targets, including promotes nuclear transfer of transcription factor EB and lysosomal repair. Here, we reviewed the recent studies on the use of natural compounds and their derivatives as autophagy regulators and discussed their potential applications in ameliorating podocyte injury. Several known natural compounds with autophagy-regulatory properties, such as quercetin, silibinin, kaempferol, and artemisinin, and their medical uses were also discussed. This review will help in improving the understanding of the podocyte protective mechanism of natural compounds and promote their development for clinical use.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:0753-3322
1950-6007
DOI:10.1016/j.biopha.2022.113670