Is mitochondrial cell fragility a cell weakness?
Advances in Experimental Medicine and Biology, ISSN: 2214-8019, Vol: 1038, Page: 107-116
2017
- 4Citations
- 6Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations4
- Citation Indexes4
- Captures6
- Readers6
Book Chapter Description
Mitochondrial dysfunction has historically been linked to the cessation of cell function and ageing. Downstream effects such as reduced calcium buffering capacity, elevated levels of reactive oxygen species, and alterations in adenosine-5′-triphosphate are linked to a wide variety of pathological diseases. The importance of the mitochondria has increasingly been highlighted due to its potential as a therapeutic target for drug intervention and cell elimination in cancer. In addition, due to its origin, drugs targeting bacteria are required to be thoroughly tested prior to administration to prevent toxicity for the mitochondria. In this chapter, we will discuss a variety of factors that could influence mitochondrial dysfunction and highlight potential solutions to these. A comprehensive understanding regarding the mechanisms underlying mitochondrial dysfunction could aid in developing future therapeutic targets in multiple pathologies such as cancer and liver diseases.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85035225981&origin=inward; http://dx.doi.org/10.1007/978-981-10-6674-0_8; http://www.ncbi.nlm.nih.gov/pubmed/29178072; http://link.springer.com/10.1007/978-981-10-6674-0_8; https://dx.doi.org/10.1007/978-981-10-6674-0_8; https://link.springer.com/chapter/10.1007/978-981-10-6674-0_8
Springer Nature
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