Mitophagy Pathways in Health and Disease

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: closed (31 August 2020) | Viewed by 10817

Special Issue Editors


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Guest Editor
Department of Biochemistry, Faculty of Medicine, University of Toronto, Toronto, ON M5G 1M1, Canada
Interests: mitophagy; parkinson disease; rhomboid protease

E-Mail Website
Guest Editor
Department of Molecular Genetics, Faculty of Medicine, University of Toronto, Toronto, ON M5G 1M1, Canada
Interests: mitochondria; drosophila; germline

Special Issue Information

Dear Colleagues,

Mitochondria are critical regulators of cellular life and death through their metabolic and apoptotic pathways, respectively. Damage to mitochondrial lipids, proteins, and DNA is an occupational hazard as a consequence of energy production within the organelle. However, the cell has evolved elegant mechanisms to deal with this accumulation of damaged mitochondria, collectively termed mitophagy. Mitophagy is the selective removal of dysfunctional mitochondria via the autophagy pathway.

In this Special Issue entitled “Mitophagy Pathways in Health and Disease”, we invite the submission of original scientific reports, review articles, commentary and perspective pieces on the broad topic of mitophagy. We seek to cover the many and varied mitophagy pathways that have been characterized to date, including basic pathway dissection in model organisms and more translational studies involving human disease mechanisms. 

We trust this Special Issue will be a comprehensive collection of articles and an incredible resource for scientists both within the field of mitochondrial biology and for life science researchers in general.

Dr. G. Angus McQuibban
Dr. Thomas Hurd
Guest Editors

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Keywords

  • mitophagy
  • neurodegeneration
  • models of human disease

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Published Papers (2 papers)

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Review

34 pages, 1860 KiB  
Review
Genetic Neuropathy Due to Impairments in Mitochondrial Dynamics
by Govinda Sharma, Gerald Pfeffer and Timothy E. Shutt
Biology 2021, 10(4), 268; https://doi.org/10.3390/biology10040268 - 26 Mar 2021
Cited by 5 | Viewed by 4745
Abstract
Mitochondria are dynamic organelles capable of fusing, dividing, and moving about the cell. These properties are especially important in neurons, which in addition to high energy demand, have unique morphological properties with long axons. Notably, mitochondrial dysfunction causes a variety of neurological disorders [...] Read more.
Mitochondria are dynamic organelles capable of fusing, dividing, and moving about the cell. These properties are especially important in neurons, which in addition to high energy demand, have unique morphological properties with long axons. Notably, mitochondrial dysfunction causes a variety of neurological disorders including peripheral neuropathy, which is linked to impaired mitochondrial dynamics. Nonetheless, exactly why peripheral neurons are especially sensitive to impaired mitochondrial dynamics remains somewhat enigmatic. Although the prevailing view is that longer peripheral nerves are more sensitive to the loss of mitochondrial motility, this explanation is insufficient. Here, we review pathogenic variants in proteins mediating mitochondrial fusion, fission and transport that cause peripheral neuropathy. In addition to highlighting other dynamic processes that are impacted in peripheral neuropathies, we focus on impaired mitochondrial quality control as a potential unifying theme for why mitochondrial dysfunction and impairments in mitochondrial dynamics in particular cause peripheral neuropathy. Full article
(This article belongs to the Special Issue Mitophagy Pathways in Health and Disease)
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25 pages, 2484 KiB  
Review
Mitophagy: A New Player in Stem Cell Biology
by George Cairns, Madhavee Thumiah-Mootoo, Yan Burelle and Mireille Khacho
Biology 2020, 9(12), 481; https://doi.org/10.3390/biology9120481 - 19 Dec 2020
Cited by 19 | Viewed by 5308
Abstract
The fundamental importance of functional mitochondria in the survival of most eukaryotic cells, through regulation of bioenergetics, cell death, calcium dynamics and reactive oxygen species (ROS) generation, is undisputed. However, with new avenues of research in stem cell biology these organelles have now [...] Read more.
The fundamental importance of functional mitochondria in the survival of most eukaryotic cells, through regulation of bioenergetics, cell death, calcium dynamics and reactive oxygen species (ROS) generation, is undisputed. However, with new avenues of research in stem cell biology these organelles have now emerged as signaling entities, actively involved in many aspects of stem cell functions, including self-renewal, commitment and differentiation. With this recent knowledge, it becomes evident that regulatory pathways that would ensure the maintenance of mitochondria with state-specific characteristics and the selective removal of organelles with sub-optimal functions must play a pivotal role in stem cells. As such, mitophagy, as an essential mitochondrial quality control mechanism, is beginning to gain appreciation within the stem cell field. Here we review and discuss recent advances in our knowledge pertaining to the roles of mitophagy in stem cell functions and the potential contributions of this specific quality control process on to the progression of aging and diseases. Full article
(This article belongs to the Special Issue Mitophagy Pathways in Health and Disease)
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