Targeting mitochondrial dysfunction: an innovative strategy for treating renal fibrosis

Area of Science:

• Nephrology
• Cell Biology
• Mitochondrial Biology

Background:

• Kidney disease incidence, particularly end-stage renal disease, is rising globally.
• Mitochondrial dysfunction impairs cellular energy metabolism and increases oxidative stress in kidneys.
• Mitochondrial quality control is crucial for preventing renal fibrosis (RF).

Purpose of the Study:

• To review the molecular mechanisms of mitochondrial damage in renal fibrosis.
• To explore the role of mitochondrial dysfunction in RF pathogenesis.
• To provide a basis for novel therapeutic strategies against RF.

Main Methods:

• Systematic review of existing literature.
• Elaboration of molecular mechanisms linking mitochondrial dysfunction and RF.
• Analysis of cellular processes involved in RF, including podocyte injury, cell transdifferentiation, fibroblast activation, and macrophage infiltration.

Main Results:

• Mitochondrial dysfunction is a key factor in renal fibrosis progression.
• Disturbances in mitochondrial dynamics, autophagy, oxidative stress regulation, and biosynthesis are implicated in RF.
• Mitochondrial damage plays a significant role in the multicellular pathological process of RF.

Conclusions:

• Mitochondrial dysfunction is central to the development and progression of renal fibrosis.
• Targeting mitochondrial pathways offers potential therapeutic avenues for kidney disease.
• Further research into mitochondrial mechanisms can lead to strategies for delaying RF advancement.