Mitochondrial Dynamics: Fusion and Fission

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Mitochondria".

Deadline for manuscript submissions: closed (28 February 2020) | Viewed by 909

Special Issue Editor

Department of Internal Medicine, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430-6540, USA
Interests: aging; mitochondrial dynamics; oxidative stress; mitophagy; neurodegeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The purpose of this Special Issue on ‘Mitochondrial Dynamics: Fusion and Fission’ is to discuss recent developments in mitochondrial dynamics in aging, cancer, cardiovascular, diabetes/obesity, age-related neurodegenerative diseases, and inherited mitochondrial diseases. Mitochondrial dynamics is a delicate balance between division and fusion. In healthy cells, fission and fusion events balance equally, which maintains mitochondrial function. Mitochondria are synthesized in the cell body and travel along axons and dendrites to supply energy to nerve terminals for normal neural communication. In this process, mitochondria alter their shape and size, which facilitates their movement from the cell body to axons, dendrites, and synapses, and back to the cell body. Mitochondria fission is controlled by evolutionary conserved, dynamin-related large GTPases. Fission is regulated by Drp1 and by Fis1, the latter of which is localized in the outer membrane of the mitochondria. When a mitochondrion signals to divide, Drp1 translocates to the outer membrane of the mitochondria, where it initiates the process of fragmentation. By contrast, mitochondria fusion is controlled by 3 GTPase proteins: Mfn1 and Mfn2, which are located in the mitochondrial outer membrane, and Opa1, which is located in the mitochondrial inner membrane. The C-terminal portion of Mfn1 mediates oligomerization between Mfn molecules of adjacent mitochondria, facilitating mt fusion. Recent studies have found increased mitochondrial fission and reduced fusion, suggesting that impaired mitochondrial dynamics is present in aging and age-related neurodegenerative disease. The articles from this Special Issue will provide new information about mitochondrial dynamics, mitochondrial dysfunction, and mitophagy in aging and other human diseases.

Prof. P. Hemachandra Reddy
Guest Editor

Manuscript Submission Information

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Keywords

  • aging
  • mitochondrial dynamics
  • oxidative stress
  • mitophagy
  • neurodegeneration

Published Papers

There is no accepted submissions to this special issue at this moment.
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