Artemether attenuates renal tubular injury by targeting mitochondria in adriamycin nephropathy mice

Xinyuan Cheng1, Peng Zhou1, Wenci Weng1

  • 1Department of Nephrology, Shenzhen Traditional Chinese Medicine Hospital, The Fourth Clinical Medical College of Guangzhou University of Chinese Medicine Shenzhen, Guangdong, China.

Insights

Artemether protects kidneys by improving mitochondrial function and biogenesis in renal tubules, offering a potential treatment for chronic kidney disease and renal tubular injury.

Area of Science:

  • Nephrology
  • Mitochondrial Biology
  • Pharmacology

Background:

  • Chronic kidney disease (CKD) pathogenesis involves complex mechanisms, with renal tubular injury and fibrosis being key drivers of progression.
  • Mitochondrial dysfunction in renal tubules is increasingly recognized as a significant contributor to kidney disease.
  • The precise mechanisms underlying the renal protective effects of artemether remain largely undefined.

Purpose of the Study:

  • To investigate the therapeutic potential of artemether in mitigating renal tubular injury and fibrosis.
  • To elucidate the role of artemether in regulating mitochondrial function and biogenesis within renal tubules.
  • To explore artemether's impact on apoptosis-related proteins (Bax and Bcl-xL) and pyruvate metabolism in the context of kidney injury.

Main Methods:

  • In vivo studies involving animal models of kidney disease to assess artemether's effects on renal function and histology.
  • In vitro experiments using cell cultures to examine artemether's direct impact on renal tubular cells.
  • Analysis of urinary protein/creatinine ratio, renal tubular morphology, mitochondrial pyruvate metabolism, mitochondrial biogenesis, and expression of apoptosis-related proteins.

Main Results:

  • Artemether treatment significantly reduced urinary protein/creatinine ratio and attenuated renal tubular injury.
  • Both in vivo and in vitro data demonstrated that artemether restored altered renal tubular phenotypes.
  • Artemether normalized the expression of Bax and Bcl-xL, regulated mitochondrial pyruvate metabolism, enhanced mitochondrial biogenesis, and improved overall mitochondrial function.

Conclusions:

  • Artemether effectively attenuates renal tubular injury and fibrosis by enhancing mitochondrial biogenesis and function.
  • The drug demonstrates potential in restoring cellular homeostasis and regulating apoptotic pathways in damaged renal tubules.
  • Artemether shows promise as a clinical therapeutic agent for kidney diseases, particularly those characterized by renal tubular injury.

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