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NDP52 and its emerging role in pathogenesis
Krenare Bruqi1, Flavie Strappazzon2
1Univ Lyon, Univ Lyon 1, CNRS, INSERM, Physiopathologie et Génétique du Neurone et du muscle, UMR5261, U1315, Institut Neuromyogène, Lyon, France.
Cell Death & Disease
|May 3, 2025
Summary
NDP52 acts as a cellular bridge, linking damaged components to autophagy for renewal. Variants of NDP52 influence inflammatory diseases like Crohn's, MS, and Alzheimer's, suggesting therapeutic potential.
Area of Science:
- Cellular Biology
- Molecular Biology
- Immunology
Background:
- Autophagy is essential for cellular homeostasis, involving selective degradation of cellular components.
- Autophagy receptors link cargo to the autophagic machinery for targeted removal.
- NDP52 (CALCOCO2) is an autophagy receptor involved in mitophagy, xenophagy, and aggrephagy.
Purpose of the Study:
- To review the functions of NDP52 in cellular processes.
- To highlight the role of NDP52 variants in inflammatory diseases.
- To explore NDP52 as a potential therapeutic target for neurodegenerative and autoimmune diseases.
Main Methods:
- Literature review of autophagy mechanisms.
- Analysis of NDP52's role in selective autophagy pathways.
- Examination of genetic studies linking NDP52 variants to disease risk.
Main Results:
- NDP52 functions as a crucial adaptor in mitophagy, xenophagy, and aggrephagy.
- Specific human NDP52 variants are associated with risk or protection in Crohn's disease, Multiple Sclerosis, and Alzheimer's disease.
- Shared pathological features in these diseases involve mitochondrial dysfunction, gut microbiota imbalance, and infections.
Conclusions:
- NDP52 plays a central role in cellular quality control and immunity.
- NDP52 variants may influence disease susceptibility through inflammatory pathways.
- Targeting NDP52 offers potential for novel therapeutic strategies against inflammatory diseases.
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