Special Issue "Mitochondrial Redox Regulations"
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 17657
Mitochondria are recognized as a metabolic hub, but also as the redox hub, controlling cell fate and emanating superoxide/H2O2, which in a regulated form can be regarded as redox signaling. Retrograde redox signaling from the mitochondrion can be directed towards the cell cytosol, nucleus, plasma membrane or other cell components. It is executed via the H2O2 diffusion or by redox relaying enzymes, such as peroxiredoxins. In addition to redox-sensitive kinases and phosphatases, prominent receivers of the redox signal are extracellular matrix metaloproteinases, redox-sensitive channels and, upon hypoxia, also inhibitable proline hydroxylase domain enzymes (PHD/EglN, plus FIH), leading to HIF-1α accumulation and resulting transcriptome reprogramming. An opposite redox signaling direction is represented by the external redox signaling from the cell towards the mitochondrion, including H2O2 activation of kinases within the intracristal space, likewise leading to, e.g., sulfenylation of critical cysteines in mitochondrial proteins. Finally, intra-mitochondrial redox signaling exists just within the interior of the outer mitochondrial membrane, exemplified by acetylation of MnSOD making it inactive, or by the H2O2-activated phospholipase iPLA2γ; and by a plethora of situations of elevated superoxide leading to the initiation of apoptosis. Coverage of these topics is welcome for this Special Issue, including both reviews and experimental articles.
Prof. Dr. Petr Ježek
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- Redox signaling to and from mitochondrion
- Physiological mitochondrial redox homeostasis
- Mitochondrial redox biology of diseases