Mitochondrial dysfunction in fibrotic diseases: Research progress and MSC-exos therapy

Area of Science:

• Cell Biology
• Pathology
• Translational Medicine

Background:

• Fibrosis is a hallmark of end-stage chronic diseases, yet its pathogenesis and treatments remain elusive.
• Mitochondria, crucial for cellular energy and homeostasis, are increasingly implicated in fibrotic disease development.
• Mitochondrial dysfunction is a key factor in the onset and advancement of fibrosis.

Purpose of the Study:

• To review the intricate links between mitochondrial dysfunction and fibrosis progression.
• To explore the roles of mitophagy, oxidative stress, mitochondrial dynamics, and mtDNA release in fibrosis.
• To summarize current research on mitochondrial dysfunction in lung, liver, kidney, and skin fibrosis.

Main Methods:

• Literature review synthesizing current research on mitochondrial dysfunction in fibrotic diseases.
• Analysis of the relationship between mitochondrial processes (mitophagy, dynamics, mtDNA release) and fibrosis.
• Overview of potential therapeutic applications of mesenchymal stem cell-derived exosomes.

Main Results:

• Mitochondrial dysfunction, including impaired mitophagy, increased oxidative stress, altered dynamics, and mtDNA release, is strongly associated with fibrosis.
• Specific examples of mitochondrial dysfunction's role in lung, liver, kidney, and skin fibrosis are detailed.
• Mesenchymal stem cell-derived exosomes show promise for treating fibrosis by enhancing mitochondrial function.

Conclusions:

• Mitochondrial dysfunction is a critical mediator in the pathogenesis of diverse fibrotic diseases.
• Targeting mitochondrial pathways presents a promising therapeutic avenue for fibrotic conditions.
• Mesenchymal stem cell-derived exosomes offer a novel strategy for fibrotic disease treatment via mitochondrial repair.