Renal fibrosis is a key pathological change that occurs in the progression of almost all chronic kidney diseases . CKD has the characteristics of high morbidity and mortality. Its prevalence is increasing each year on a global scale, which seriously affects people's health and quality of life. Natural products have been used for new drug development and disease treatment for many years. The abundant natural products in . can intervene in the process of renal fibrosis in different ways and have considerable therapeutic prospects. The etiology and pathology of renal fibrosis were analyzed, and the different ways in which the natural components of . can intervene and provide curative effects on the process of renal fibrosis were summarized. Methods: Electronic databases, such as PubMed, Life Science, MEDLINE, and Web of Science, were searched using the keywords '.', 'kidney fibrosis', 'emodin' and 'rhein', and the various ways in which the natural ingredients protect against renal fibrosis were collected and sorted out. We analyzed several factors that play a leading role in the pathogenesis of renal fibrosis, such as the mechanism of the TGF-β/Smad and Wnt/β-catenin signaling pathways. Additionally, we reviewed the progress of the treatment of renal fibrosis with natural components in . and the intervention mechanism of the crucial therapeutic targets. The natural components of . have a wide range of intervention effects on renal fibrosis targets, which provides new ideas for the development of new anti-kidney fibrosis drugs.
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http://dx.doi.org/10.3389/fphar.2022.919967 | DOI Listing |
J Diabetes Investig
January 2025
Faculty of Medicine, Internal Medicine, Shimane University, Izumo, Shimane, Japan.
Aim/introduction: Senescence is a key driver of age-related kidney dysfunction, including diabetic kidney disease. Oxidative stress activates cellular senescence, induces abnormal glycolysis, and is associated with pyruvate kinase muscle isoform 2 (PKM2) dysfunction; however, the mechanisms linking PK activation to cellular senescence have not been elucidated. We hypothesized that PKM2 activation by TEPP-46 could suppress oxidative stress-induced renal tubular cell injury and cellular senescence.
View Article and Find Full Text PDFQuant Imaging Med Surg
January 2025
Department of Ultrasound, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
Background: Traditional 2-dimensional (2D) ultrasound is a noninvasive method in the assessment of glomerular disease. Ultrasound elastography shows promise in evaluating renal fibrosis, which plays a key role in glomerular disease progression. However, research in pediatric cohorts is limited.
View Article and Find Full Text PDFRedox Biol
January 2025
Department of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan, 430060, China. Electronic address:
Objective: This study investigates the effects of caloric restriction (CR) on renal injury and fibrosis following ischemia-reperfusion injury (IRI), with a focus on the roles of the mechanistic/mammalian target of rapamycin complex 1 (mTORC1) signaling and autophagy.
Methods: A mouse model of unilateral IRI with or without CR was used. Renal function was assessed through serum creatinine and blood urea nitrogen levels, while histological analysis and molecular assays evaluated tubular injury, fibrosis, mTORC1 signaling, and autophagy activation.
Adv Sci (Weinh)
January 2025
Department of Nephrology, Xiangya Hospital, Central South University, Changsha, 410008, China.
Renal fibrosis is a common pathway involved in the progression of various chronic kidney diseases to end-stage renal disease. Recent studies show that mitochondrial injury of renal tubular epithelial cells (RTECs) is a crucial pathological foundation for renal fibrosis. However, the underlying regulatory mechanisms remain unclear.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Division of Nephrology, Duke University, Durham, United States of America.
The role of macrophages remains incompletely understood in kidney injury and repair. Their plasticity offers an opportunity to polarize them towards mediating injury resolution in both native and transplanted kidneys undergoing ischemia and/or rejection. Here, we show that infiltrating kidney macrophages augmented their AIF-1 expression after injury.
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