Induction of autophagy by depolarization of mitochondria

Lyamzaev, K.; Tokarchuk, A.; Panteleeva, A.; Mulkidjanian, A.; Skulachev, V.; Chernyak, B.

Статья опубликована в высокорейтинговом журнале

Информация о цитировании статьи получена из Web of Science, Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 27 марта 2018 г.

Авторы: Lyamzaev KG, Tokarchuk AV, Panteleeva AA, Mulkidjanian AY, Skulachev VP, Chernyak BV
Журнал: Autophagy
Год издания: 2018
Издательство: Landes Bioscience
Местоположение издательства: United States
Первая страница: 1
Последняя страница: 8
DOI: 10.1080/15548627.2018.1436937
Аннотация: Mitochondrial dysfunction plays a crucial role in the macroautophagy/autophagy cascade. In a recently published study Sun et al. described the induction of autophagy by the membranophilic triphenylphosphonium (TPP)-based cation 10-(6′-ubiquinonyl) decyltriphenylphosphonium (MitoQ) in HepG2 cells (Sun C, et al. "MitoQ regulates autophagy by inducing a pseudo-mitochondrial membrane potential (PMMP)", Autophagy 2017, 13:730-738.). Sun et al. suggested that MitoQ adsorbed to the inner mitochondrial membrane with its cationic moiety remaining in the intermembrane space, adding a large number of positive charges and establishing a “pseudo-mitochondrial membrane potential”, which blocked the ATP synthase. Here we argue that the suggested mechanism for generation of the “pseudo-mitochondrial membrane potential” is physically implausible and contradicts earlier findings on the electrophoretic displacements of membranophilic cations within and through phospholipid membranes. We provide evidence that TPP-cations dissipated the mitochondrial membrane potential in HepG2 cells and that the induction of autophagy in carcinoma cells by TPP-cations correlated with the uncoupling of oxidative phosphorylation. The mild uncoupling of oxidative phosphorylationby various mitochondria-targeted penetrating cations may contribute to their reported therapeutic effects via inducing both autophagy and mitochondria-selective mitophagy.
Добавил в систему: Лямзаев Константин Геннадьевич

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