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- W4313236994 endingPage "1891" @default.
- W4313236994 startingPage "1891" @default.
- W4313236994 abstract "Mitochondria calcium is a double-edged sword. While low levels of calcium are essential to maintain optimal rates of ATP production, extreme levels of calcium overcoming the mitochondrial calcium retention capacity leads to loss of mitochondrial function. In moderate amounts, however, ATP synthesis rates are inhibited in a calcium-titratable manner. While the consequences of extreme calcium overload are well-known, the effects on mitochondrial function in the moderately loaded range remain enigmatic. These observations are associated with changes in the mitochondria ultrastructure and cristae network. The present mini review/perspective follows up on previous studies using well-established cryo–electron microscopy and poses an explanation for the observable depressed ATP synthesis rates in mitochondria during calcium-overloaded states. The results presented herein suggest that the inhibition of oxidative phosphorylation is not caused by a direct decoupling of energy metabolism via the opening of a calcium-sensitive, proteinaceous pore but rather a separate but related calcium-dependent phenomenon. Such inhibition during calcium-overloaded states points towards mitochondrial ultrastructural modifications, enzyme activity changes, or an interplay between both events." @default.
- W4313236994 created "2023-01-06" @default.
- W4313236994 creator A5016265173 @default.
- W4313236994 creator A5036616317 @default.
- W4313236994 creator A5069474853 @default.
- W4313236994 date "2022-12-17" @default.
- W4313236994 modified "2023-10-10" @default.
- W4313236994 title "Calcium Overload and Mitochondrial Metabolism" @default.
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