Mitochondrial H2O2 metabolism as central event of heart complex I syndrome in early diabetes

Rukavina-Mikusic, Ivana A.; Rey, Micaela; Areán, Juan Santiago Adán; Vanasco, Virginia; Álvarez, Silvia; Valdez, Laura B.

doi:10.1016/j.freeradbiomed.2023.03.011

Cited by 2 publications

(2 citation statements)

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“…Redox signals or regulations of mt origin are also implicated in insulin resistance development in peripheral tissues [ 125 , 126 ]. Other listed examples include heart [ 127 , 128 , 129 ] and endothelial pathology [ 130 , 131 , 132 , 133 , 134 ], pulmonary hypertension [ 135 ], sepsis [ 136 ], skeletal muscle injuries (here, mt ROS signal for repair mechanisms, [ 137 , 138 ]), and NLR family pyrin domain-containing 3 (NLRP3)-related inflammatory states [ 139 , 140 , 141 ]. This list is illustrative and incomplete.…”

Section: Future Perspectivesmentioning

confidence: 99%

“…Other listed examples include heart [127][128][129] and endothelial pathology [130][131][132][133][134], pulmonary hypertension [135], sepsis [136], skeletal muscle injuries (here, mt ROS signal for repair mechanisms, [137,138]), and NLR family pyrin domain-containing 3 (NLRP3)-related inflammatory states [139][140][141]. This list is illustrative and incomplete.…”

Section: Future Perspectivesmentioning

confidence: 99%

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Pitfalls of Mitochondrial Redox Signaling Research

Ježek

2023

Antioxidants

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Redox signaling from mitochondria (mt) to the cytosol and plasma membrane (PM) has been scarcely reported, such as in the case of hypoxic cell adaptation or (2-oxo-) 2-keto-isocaproate (KIC) β-like-oxidation stimulating insulin secretion in pancreatic β-cells. Mutual redox state influence between mitochondrial major compartments, the matrix and the intracristal space, and the cytosol is therefore derived theoretically in this article to predict possible conditions, when mt-to-cytosol and mt-to-PM signals may occur, as well as conditions in which the cytosolic redox signaling is not overwhelmed by the mitochondrial antioxidant capacity. Possible peroxiredoxin 3 participation in mt-to-cytosol redox signaling is discussed, as well as another specific case, whereby mitochondrial superoxide release is diminished, whereas the matrix MnSOD is activated. As a result, the enhanced conversion to H2O2 allows H2O2 diffusion into the cytosol, where it could be a predominant component of the H2O2 release. In both of these ways, mt-to-cytosol and mt-to-PM signals may be realized. Finally, the use of redox-sensitive probes is discussed, which disturb redox equilibria, and hence add a surplus redox-buffering to the compartment, where they are localized. Specifically, when attempts to quantify net H2O2 fluxes are to be made, this should be taken into account.

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