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Aberrant Ca2+ handling in lysosomal storage disorders
Kirill Kiselyov1, Soichiro Yamaguchi, Christopher W Lyons
1Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA 15260, USA. Kiselyov@pitt.edu
Lysosomal storage diseases (LSDs) result from impaired cellular digestion via endocytosis. This review explores how calcium (Ca2+) handling is altered in LSDs, highlighting key questions in cellular pathogenesis.
Area of Science:
- Cell Biology
- Biochemistry
- Genetics
Background:
- Lysosomal storage diseases (LSDs) stem from defects in cellular digestion, specifically the processing of endocytosed material.
- These diseases impact numerous cellular functions, revealing insights into cellular integration and endocytic pathway complexities.
Purpose of the Study:
- To review recent findings on calcium (Ca2+) handling in LSDs.
- To identify critical questions regarding Ca2+ signaling and membrane transport alterations in LSDs.
- To connect these alterations to the underlying cellular pathogenesis of LSDs.
Main Methods:
- Literature review of recent research on LSDs and Ca2+ signaling.
- Analysis of existing data on membrane transport in the context of LSDs.
- Identification of knowledge gaps in cellular mechanisms.
Main Results:
- LSDs are associated with significant alterations in cellular calcium (Ca2+) handling.
- Dysregulation of Ca2+ signaling is a common feature across various LSDs.
- Impaired membrane transport is intrinsically linked to Ca2+ dyshomeostasis in LSDs.
Conclusions:
- Understanding Ca2+ handling in LSDs is crucial for elucidating cellular pathogenesis.
- Further research into Ca2+ signaling and membrane transport is needed to address knowledge gaps.
- Investigating Ca2+ dynamics may offer new therapeutic avenues for LSDs.
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