Abstract
Current research has demonstrated that mitochondrial morphology, distribution, and function are maintained by the balanced regulation of mitochondrial fission and fusion, and perturbation of the homeostasis between these processes has been related to cell or organ dysfunction and abnormal mitochondrial redistribution. Abnormal mitochondrial fusion induces the fragmentation of mitochondria from a tubular morphology into pieces; in contrast, perturbed mitochondrial fission results in the fusion of adjacent mitochondria. A member of the dynamin family of large GTPases, dynamin-related protein 1 (Drp1), effectively influences cell survival and apoptosis by mediating the mitochondrial fission process in mammals. Drp1-dependent mitochondrial fission is an intricate process regulating both cellular and organ dynamics, including development, apoptosis, acute organ injury, and various diseases. Only after clarification of the regulative mechanisms of this critical protein in vivo and in vitro will it set a milestone for preventing mitochondrial fission related pathological processes and refractory diseases.
Highlights
The mitochondrion is the main organelle for producing adenosine triphosphate (ATP) and acts as a regulator in synthesis of metabolites, phospholipids, heme, and intracellular calcium homeostasis [1]
This review mainly focuses on the detailed mechanisms and machinery of Dynamin-related protein 1 (Drp1)-dependent mitochondrial fission, and we can conclude that Drp1-dependent mitochondrial fission is an intricate process for regulating cellular and organ dynamics, including development, apoptosis, acute organ injury, and various diseases in mammals
Mitochondria are the smallest semi-autonomous system in mammals, mitochondrial morphology, distribution, and function are maintained by the balanced regulation of mitochondrial fission and fusion
Summary
The mitochondrion is the main organelle for producing adenosine triphosphate (ATP) and acts as a regulator in synthesis of metabolites, phospholipids, heme, and intracellular calcium homeostasis [1]. As a main regulator in mitochondrial fission process, Dynamin-related protein 1 (Drp1) in mammals consists of four different domains: the N-terminal GTP-binding, middle, insert B, and C-terminal GTPase effector (GED) domains [4]; insert B ( known as the variable domain) plays a critical role in the regulative process of mitochondrial fission since it binds the target membrane effectively [4]. Actin filaments are able to bind purified Drp and interact with Mff, thereby increasing the GTPase activity, whereas inhibiting actin polymerization significantly reduces Drp1-dependent mitochondrial fission [27]. Opa stabilizes mitochondrial structure and increases mitochondrial respiratory efficiency, thereby eliminating mitochondrial dysfunction and cytochrome c release in ischemic environments [37]
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