Mitochondrial Proteins: From Import and Biogenesis to Complex Functional Network

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biomacromolecules: Proteins".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 3697

Special Issue Editor


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Guest Editor
Department of Physiology and Pharmacology, Robert C. Byrd Health Sciences Center, School of Medicine, West Virginia University, Morgantown, WV 26506, USA
Interests: mitochondria; protein quality control; Lon protease; oxidative stress; metabolism; cardiotoxicity; myocardial infarction; mtDNA; cardiovascular disease; cancer

Special Issue Information

Dear Colleagues,

We know that only ~1% of mitochondrial proteins are encoded by mtDNA, and the rest of ~99% are encoded by nuclear DNA and imported into mitochondria through a regulated process, which is critical for optimal cellular function. In addition, mitochondria are not only energy-producing factories but also play vital roles in other subsidiary functions, such as calcium homeostasis, cellular signaling, regulation of heme, steroid, nucleotide, fatty acid synthesis, and apoptosis, to name a few. Therefore, understanding the role of mitochondrial proteins and their contribution to mitochondrial function is of utmost importance as most human diseases are associated with some form of mitochondrial dysfunction. Furthermore, such proteins involve various roles ranging from mitochondrial import and biogenesis to a complex functional network. Therefore, we believe that studying and understanding these mitochondrial proteins is of utmost importance in developing novel therapeutic strategies and tools to target them in human diseases. Thus, I welcome you to contribute to this Special Issue with original or review articles dealing with such mitochondrial proteins to take a step forward in targeting mitochondria in human diseases.

Dr. Venkatesh Sundararajan
Guest Editor

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Keywords

  • mitochondrial proteins
  • import
  • biogenesis
  • metabolism
  • functional network
  • oxidative stress
  • small molecules
  • mitochondrial protein quality control
  • mitophagy

Published Papers (1 paper)

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Review

16 pages, 1081 KiB  
Review
Electrophilic Aldehyde 4-Hydroxy-2-Nonenal Mediated Signaling and Mitochondrial Dysfunction
by Sudha Sharma, Papori Sharma, Tara Bailey, Susmita Bhattarai, Utsab Subedi, Chloe Miller, Hosne Ara, Srivatsan Kidambi, Hong Sun, Manikandan Panchatcharam and Sumitra Miriyala
Biomolecules 2022, 12(11), 1555; https://doi.org/10.3390/biom12111555 - 25 Oct 2022
Cited by 19 | Viewed by 3269
Abstract
Reactive oxygen species (ROS), a by-product of aerobic life, are highly reactive molecules with unpaired electrons. The excess of ROS leads to oxidative stress, instigating the peroxidation of polyunsaturated fatty acids (PUFA) in the lipid membrane through a free radical chain reaction and [...] Read more.
Reactive oxygen species (ROS), a by-product of aerobic life, are highly reactive molecules with unpaired electrons. The excess of ROS leads to oxidative stress, instigating the peroxidation of polyunsaturated fatty acids (PUFA) in the lipid membrane through a free radical chain reaction and the formation of the most bioactive aldehyde, known as 4-hydroxynonenal (4-HNE). 4-HNE functions as a signaling molecule and toxic product and acts mainly by forming covalent adducts with nucleophilic functional groups in proteins, nucleic acids, and lipids. The mitochondria have been implicated as a site for 4-HNE generation and adduction. Several studies clarified how 4-HNE affects the mitochondria’s functions, including bioenergetics, calcium homeostasis, and mitochondrial dynamics. Our research group has shown that 4-HNE activates mitochondria apoptosis-inducing factor (AIFM2) translocation and facilitates apoptosis in mice and human heart tissue during anti-cancer treatment. Recently, we demonstrated that a deficiency of SOD2 in the conditional-specific cardiac knockout mouse increases ROS, and subsequent production of 4-HNE inside mitochondria leads to the adduction of several mitochondrial respiratory chain complex proteins. Moreover, we highlighted the physiological functions of HNE and discussed their relevance in human pathophysiology and current discoveries concerning 4-HNE effects on mitochondria. Full article
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