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Targeting new cellular disease pathways in autosomal dominant polycystic kidney disease
Ming-Yang Chang1, Albert C M Ong2,3
1Kidney Research Center, Department of Nephrology, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
Abstract:
Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited cause of end-stage renal failure. Understanding the molecular and cellular pathogenesis of ADPKD could help to identify new targets for treatment. The classic cellular cystic phenotype includes changes in proliferation, apoptosis, fluid secretion, extracellular matrix and cilia function. However, recent research, suggests that the cellular cystic phenotype could be broader and that changes, such as altered metabolism, autophagy, inflammation, oxidative stress and epigenetic modification, could play important roles in the processes of cyst initiation, cyst growth or disease progression. Here we review these newer cellular pathways, describe evidence for their possible links to cystic pathogenesis or different stages of disease and discuss the options for developing novel treatments.
Insights
Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited kidney disease. Newer research reveals broader cellular changes beyond the classic phenotype, offering new therapeutic targets for ADPKD.
Area of Science:
- Nephrology
- Molecular Biology
- Genetics
Background:
- Autosomal dominant polycystic kidney disease (ADPKD) is the leading inherited cause of end-stage renal failure.
- The classic cellular cystic phenotype involves altered proliferation, apoptosis, fluid secretion, extracellular matrix, and cilia function.
- Emerging evidence suggests a broader cellular cystic phenotype in ADPKD.
Purpose of the Study:
- To review newer cellular pathways implicated in ADPKD pathogenesis.
- To explore the roles of altered metabolism, autophagy, inflammation, oxidative stress, and epigenetic modifications in ADPKD.
- To discuss potential novel therapeutic targets based on these pathways.
Main Methods:
- Literature review of recent research on ADPKD cellular pathogenesis.
- Analysis of evidence linking novel cellular pathways to cyst initiation, growth, and progression.
- Synthesis of information to identify potential therapeutic strategies.
Main Results:
- The cellular cystic phenotype in ADPKD extends beyond classic features.
- Altered metabolism, autophagy, inflammation, oxidative stress, and epigenetic modifications are increasingly recognized as critical factors.
- These pathways are implicated in various stages of ADPKD, from initiation to progression.
Conclusions:
- Understanding these expanded cellular pathways is crucial for a comprehensive view of ADPKD.
- Novel therapeutic strategies targeting metabolism, autophagy, inflammation, oxidative stress, and epigenetics hold promise for ADPKD treatment.
- Further research into these newer pathways could lead to more effective interventions for patients with ADPKD.