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Altered ER–mitochondria contact impacts mitochondria calcium homeostasis and contributes to neurodegeneration in vivo in disease models
Open accessAbstract
Significance: Ca 2 + regulates cellular metabolism, proliferation, and differentiation. Ca 2+ homeostasis is critical for cellular function and health. Mitochondria help buffer transient Ca 2+ elevations and prevent cell death induced by Ca 2+ overload. Mito-Ca 2+ is also required for optimal activity of certain key mitochondrial functions, such as oxidative phosphorylation and metabolism. Thus, mito-Ca 2+ homeostasis assumes central roles in cellular health. Endoplasmic reticulum (ER) and mitochondria make intimate contacts and exchange molecules such as Ca 2+ and lipids. We find that ER-to-mitochondria Ca 2+ transfer is important for mito-Ca 2+ homeostasis and that the conserved Miro protein is critically involved. We show that mito-Ca 2+ homeostasis is disrupted in neurodegenerative disease models and its restoration is beneficial. Our findings have important implications for therapeutic intervention of neurodegenerative diseases.
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Metadata
- Authors
- Lee, K.-S., Huh, S., Lee, S., Wu, Z., Kim, A.-K., Kang, H.-Y., & Lu, B.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2018-09-05
- Volume
- 115
- Issue
- 38
- Pages
- E8844-E8853
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2889803986
- Cited by
- 232
- References
- 10
- FWCI
- 8.79
- Type
- journal article
- Language
- en
- Open access
- green
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- Lee, K.-S., Huh, S., Lee, S., Wu, Z., Kim, A.-K., Kang, H.-Y., & Lu, B. (2018). Altered ER–mitochondria contact impacts mitochondria calcium homeostasis and contributes to neurodegeneration in vivo in disease models. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1721136115
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