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Remodeling of Mitochondria in Cancer and Other Diseases 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (15 January 2023) | Viewed by 3851

Special Issue Editor

Special Issue Information

Dear Colleagues, 

Mitochondria are highly dynamic and responsive organelles that are capable of undergoing fission and fusion and are the hub for diverse signal processors, which are fundamental to cellular homeostasis, energy production, metabolism, survival, and death. Mitochondiral remodeling, including rearranging, recycling, and reprogramming, is essential for mitochondrial quality control, structural integrity, and functional interaction with other cellular organelles. Alhtough we are still far from fully understanding the complexity of mitochondrial remodeling in its physiological and pathophysiological significance, this process has been, nonetheless, implicated in the pathogenesis of many human disorders, including cancer and aging-related diseases. With the advent of new information, technologies, and methodologies, it is time to delineate the significance and enigmatic mechanisms relevant to the dynamic remodeling of mitochondria in response to pathophysiological stresses in a more precise and comprehensive way. In this respect, scientific evidence and provocative ideas are important to translate science into practice effectively. Therefore, we kindly invite you to contribute to this Special Issue with original research articles or comprehensive reviews on all molecular aspects related to the theme of “Remodeling of Mitochondria in Cancer and Other Diseases”. Short perspective papers or pure clinical papers will not be considered, while novel Communication articles with interesting molecular data will be of interest. This Special Issue aims to increase our understanding of the role, regulation, and impact of mitochondrial remodeling in disease-specific pathology and possibly translate these finding into therapeutics, from basic research to the clinic.

Dr. Yong Teng
Guest Editor

Manuscript Submission Information

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Keywords

  • mitochondrial biology
  • mitochondrial remodeling
  • mitochondrial biogenesis and bioenergetics
  • mitochondrial dynamic network
  • cancer development and progression
  • mitochodria-associated human diseases
  • mitochondria communication
  • targeting mitochondria
  • mitochondrial oncolgoy

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Published Papers (1 paper)

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Research

14 pages, 1948 KiB  
Article
Uremic Myopathy and Mitochondrial Dysfunction in Kidney Disease
by Eurico Serrano, Diana Whitaker-Menezes, Zhao Lin, Megan Roche and Maria Paula Martinez Cantarin
Int. J. Mol. Sci. 2022, 23(21), 13515; https://doi.org/10.3390/ijms232113515 - 4 Nov 2022
Cited by 3 | Viewed by 3156
Abstract
Alterations in muscle structure and function in chronic kidney disease (CKD) patients are associated with poor outcomes. As key organelles in muscle cell homeostasis, mitochondrial metabolism has been studied in the context of muscle dysfunction in CKD. We conducted a study to determine [...] Read more.
Alterations in muscle structure and function in chronic kidney disease (CKD) patients are associated with poor outcomes. As key organelles in muscle cell homeostasis, mitochondrial metabolism has been studied in the context of muscle dysfunction in CKD. We conducted a study to determine the contribution of oxidative metabolism, glycolysis and fatty acid oxidation to the muscle metabolism in CKD. Mice developed CKD by exposure to adenine in the diet. Muscle of CKD mice showed significant weight loss compared to non-CKD mice, but only extensor digitorum longus (EDL) muscle showed a decreased number of fibers. There was no difference in the proportion of the various muscle fibers in CKD and non-CKD mice. Muscle of CKD mice had decreased expression of proteins associated with oxidative phosphorylation but increased expression of enzymes and transporters associated with glycolysis. In cell culture, myotubes exposed to uremic serum demonstrated decreased oxygen consumption rates (OCR) when glucose was used as substrate, conserved OCR when fatty acids were used and increased lactate production. In conclusion, mice with adenine-induced CKD developed sarcopenia and with increased glycolytic metabolism but without gross changes in fiber structure. In vitro models of uremic myopathy suggest fatty acid utilization is preserved compared to decreased glucose utilization. Full article
(This article belongs to the Special Issue Remodeling of Mitochondria in Cancer and Other Diseases 2.0)
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