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Exploring Cathepsin K as the Mechanistic Link Between Disrupted Lysosomal Acidification and Microglial Dysfunction

Year: 2026

Type: article

Abstract: As proper lysosomal acidification, driven by Vacuolar-ATPases, is essential for microglial function, understanding how microglial function can be impaired by a loss of lysosomal acidification is broadly important and therapeutically relevant. I found that mutants with a loss of lysosomal acidification (atp6ap2 -/-) have less mature active cathepsin K and more preprocathepsin K when compared to siblings with normal lysosomal acidification (atp6ap2 +/+; +/-). Additionally, zebrafish larvae with normal lysosomal acidification show aggregation of cathepsin K within microglia, while atp6ap2 mutants have no detectable cathepsin K protein.

Source: UNC Libraries

DOI: 10.17615/576w-2545

Author: Jinglun Wang

Institution: University of North Carolina at Chapel Hill

Language: English

Topic: Neuroinflammation and Neurodegeneration Mechanisms

Subfield: Neurology

Field: Neuroscience

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: green

OpenAlex ID: W7203899750

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