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CoA in Health and Disease 3.0

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

Deadline for manuscript submissions: 20 February 2025 | Viewed by 2932

Special Issue Editor


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Guest Editor
Laboratory of Molecular Medical Biochemistry, Nencki Institute of Experimental Biology of Polish Academy of Sciences, 02-093 Warsaw, Poland
Interests: physiology; endocrinology; metabolism; lipids; lipogenesis; lipolysis; stearoyl-CoA desaturase; angiogenesis; cardiovascular system; mitochondria; obesity; type 2 diabetes; transcription factors
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Special Issue Information

Dear Colleagues,

CoA and its thioester derivatives are crucial components of numerous biosynthetic and degradative pathways of cellular metabolism (including the synthesis and oxidation of fatty acids, the Krebs cycle, ketogenesis, the biosynthesis of cholesterol and acetylcholine, and the degradation of amino acids), post-translational modifications of proteins, and the regulation of gene expression. Consequently, it is not surprising that the abnormal biosynthesis of CoA/CoA derivatives is associated with numerous pathologies, including diabetes, neurodegeneration, Reye’s syndrome, vitamin B12 deficiency, cardiac hypertrophy, and cancer. This Special Issue of the IJMS will showcase selected novel research articles covering the multiple roles of CoA and its derivatives in extracellular and intracellular signaling functions in physiology and pathology.

Topics of interest to this Special Issue include, but are not limited to, the following:

  • CoA synthesis and degradation;
  • CoA transport and mitochondria;
  • Extracellular functions of CoA/CoA thioesters;
  • CoA/CoA thioesters as intracellular signaling molecules;
  • Physiological and pathological changes in cellular CoA concentrations;
  • Interconversion between CoA and its thioester derivatives in health and disease;
  • The roles of nutrients, hormones, and other factors in the regulation of CoA levels in cells;
  • Acyl-CoA metabolism;
  • Association of CoA/acyl-CoA with fatty acid metabolism.

In addition, critical reviews of the status and perspectives regarding the role of CoA in pathophysiology are welcomed.

Dr. Pawel Dobrzyn
Guest Editor

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Keywords

  • energy production
  • impaired metabolism
  • Acyl-CoA synthesis and function
  • Acetyl-CoA
  • CoA analogues
  • oxidative stress
  • hereditary diseases

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Published Papers (2 papers)

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12 pages, 1927 KiB  
Article
Two Regions with Different Expression of Lipogenic Enzymes in Rats’ Posterior Subcutaneous Fat Depot
by Jacek Turyn, Ewa Stelmanska and Sylwia Szrok-Jurga
Int. J. Mol. Sci. 2024, 25(21), 11546; https://doi.org/10.3390/ijms252111546 - 27 Oct 2024
Viewed by 638
Abstract
Lipid metabolism in various adipose tissue depots can differ vastly. This also applies to lipogenesis, the process of synthesizing fatty acids from acetyl-CoA. This study compared the expression of some lipogenic enzymes: fatty acid synthase (FASN), ATP-citrate lyase (ACLY), and malic enzyme 1 [...] Read more.
Lipid metabolism in various adipose tissue depots can differ vastly. This also applies to lipogenesis, the process of synthesizing fatty acids from acetyl-CoA. This study compared the expression of some lipogenic enzymes: fatty acid synthase (FASN), ATP-citrate lyase (ACLY), and malic enzyme 1 (ME1) in different regions of the posterior subcutaneous adipose tissue in rats. Methods and Results: Posterior subcutaneous adipose tissue collected from twelve-month-old Wistar rats was divided into six parts (A–F). The expression of genes encoding lipogenic enzymes was assessed by measuring their activity and mRNA levels using real-time PCR. In the gluteal region of the fat pad, there were much higher levels of activity and mRNA for these lipogenic enzymes compared to the dorsolumbar region. The mRNA level of FASN increased by more than twentyfold, whereas the level of ME1 and ACLY increased eight- and fivefold respectively. This phenomenon was observed in both old and young animals. Furthermore, the lack of uncoupling protein one (Ucp1) expression suggests that neither the presence of brown adipocytes in the gluteal part nor the transformation of white adipocytes into beige contributed to the observed differences. Conclusion: These results indicate that the gluteal white adipose tissue appears to be a unique and separate subcutaneous fat depot. Full article
(This article belongs to the Special Issue CoA in Health and Disease 3.0)
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Review

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19 pages, 4232 KiB  
Review
Involvement of Type 10 17β-Hydroxysteroid Dehydrogenase in the Pathogenesis of Infantile Neurodegeneration and Alzheimer’s Disease
by Xue-Ying He, Jannusz Frackowiak, Carl Dobkin, William Ted Brown and Song-Yu Yang
Int. J. Mol. Sci. 2023, 24(24), 17604; https://doi.org/10.3390/ijms242417604 - 18 Dec 2023
Cited by 1 | Viewed by 1770
Abstract
Type 10 17β-hydroxysteroid dehydrogenase (17β-HSD10) is the HSD17B10 gene product playing an appreciable role in cognitive functions. It is the main hub of exercise-upregulated mitochondrial proteins and is involved in a variety of metabolic pathways including neurosteroid metabolism to regulate allopregnanolone homeostasis. Deacetylation [...] Read more.
Type 10 17β-hydroxysteroid dehydrogenase (17β-HSD10) is the HSD17B10 gene product playing an appreciable role in cognitive functions. It is the main hub of exercise-upregulated mitochondrial proteins and is involved in a variety of metabolic pathways including neurosteroid metabolism to regulate allopregnanolone homeostasis. Deacetylation of 17β-HSD10 by sirtuins helps regulate its catalytic activities. 17β-HSD10 may also play a critical role in the control of mitochondrial structure, morphology and dynamics by acting as a member of the Parkin/PINK1 pathway, and by binding to cyclophilin D to open mitochondrial permeability pore. 17β-HSD10 also serves as a component of RNase P necessary for mitochondrial tRNA maturation. This dehydrogenase can bind with the Aβ peptide thereby enhancing neurotoxicity to brain cells. Even in the absence of Aβ, its quantitative and qualitative variations can result in neurodegeneration. Since elevated levels of 17β-HSD10 were found in brain cells of Alzheimer’s disease (AD) patients and mouse AD models, it is considered to be a key factor in AD pathogenesis. Since data underlying Aβ-binding-alcohol dehydrogenase (ABAD) were not secured from reported experiments, ABAD appears to be a fabricated alternative term for the HSD17B10 gene product. Results of this study would encourage researchers to solve the question why elevated levels of 17β-HSD10 are present in brains of AD patients and mouse AD models. Searching specific inhibitors of 17β-HSD10 may find candidates to reduce senile neurodegeneration and open new approaches for the treatment of AD. Full article
(This article belongs to the Special Issue CoA in Health and Disease 3.0)
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