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Updated: Jun 6, 2026

Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry
Published on: October 28, 2014
Endolysosomal calcium regulation and disease
Emyr Lloyd-Evans1, Helen Waller-Evans, Ksenia Peterneva
1Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK. lloyd-evanse@cardiff.ac.uk
Endolysosomal calcium regulation is crucial for cellular function. This review explores how disruptions in calcium release mechanisms, particularly involving nicotinic acid-adenine dinucleotide phosphate (NAADP), contribute to metabolic disorders like Niemann-Pick type C.
Area of Science:
- Cell Biology
- Biochemistry
- Physiology
Background:
- Endolysosomal calcium homeostasis mechanisms were previously unclear.
- Two-pore channels are key molecular targets for NAADP in the endolysosomal system, identifying it as a critical calcium store.
- Dysfunctional NAADP release impairs endocytic function, leading to lipid accumulation in Niemann-Pick type C disease.
Purpose of the Study:
- To summarize current knowledge on endolysosomal calcium homeostasis.
- To investigate the link between endolysosomal calcium dysregulation and human metabolic disorders.
Main Methods:
- Literature review of recent findings on endolysosomal calcium signaling.
- Analysis of the role of NAADP and two-pore channels in cellular calcium regulation.
- Examination of connections between calcium homeostasis defects and metabolic diseases.
Main Results:
- NAADP-sensitive two-pore channels are central to endolysosomal calcium storage and release.
- Defective lysosomal calcium release is directly linked to Niemann-Pick type C disease pathogenesis.
- Endolysosomal calcium signaling plays a significant role in cellular lipid metabolism.
Conclusions:
- Endolysosomal calcium homeostasis is vital for proper endocytic function and preventing lipid accumulation.
- Disruptions in NAADP-mediated calcium release are implicated in human metabolic disorders.
- Further research into endolysosomal calcium regulation may reveal new therapeutic targets for metabolic diseases.
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