Mitochondrial Medicine: A Themed Issue in Honor of Prof. Dr. Carl A. Pinkert

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 653

Special Issue Editor


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Guest Editor
Institute for Physical Activity and Nutrition, School of Life and Environmental Sciences, Deakin University, Waurn Ponds, VIC, Australia
Interests: mitochondrial function; mitochondrial disease; stem cells; metabolism

Special Issue Information

Dear Colleagues,

I would like to invite you to contribute a manuscript to this Special Issue in honor of Prof. Carl A. Pinkert. Prof. Pinkert’s research has employed molecular biotechnology and animal transgenics to model human disease, and his work has made a significant contribution to our understanding of disease pathogenesis. Prof. Pinkert has generated various animal models of mitochondrial dysfunction that have provided new insights into the molecular mechanisms involved in these diseases.

Manuscripts for this Special Issue can be reviews, opinions or original research papers, and should align with Prof. Pinkert’s research interests over his career. This includes mitochondrial disease, mitochondrial DNA (mtDNA) genetics and mitochondrial medicine. Diseases of interest can encompass both ‘classical’ mitochondrial disorders as well as human diseases where mitochondrial dysfunction has been identified as an important contributor to disease pathogenesis (for example, neurodegenerative disorders).

Our field is now utilizing its knowledge of mitochondrial biology to develop novel treatments that target specific deficiencies in mitochondrial function. This Special Issue will focus on the seminal work being undertaken in this area.

Dr. Matthew McKenzie
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondrial biology
  • mitochondrial disease
  • mitochondrial DNA
  • mitochondrial medicine
  • metabolism
  • therapeutics
  • oxidative phosphorylation
  • reactive oxygen species

Published Papers (1 paper)

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Research

21 pages, 4114 KiB  
Article
Mitochondrial DNA and Inflammation Are Associated with Cerebral Vessel Remodeling and Early Diabetic Kidney Disease in Patients with Type 2 Diabetes Mellitus
by Ligia Petrica, Florica Gadalean, Danina Mirela Muntean, Dragos Catalin Jianu, Daliborca Vlad, Victor Dumitrascu, Flaviu Bob, Oana Milas, Anca Suteanu-Simulescu, Mihaela Glavan, Sorin Ursoniu, Lavinia Balint, Maria Mogos-Stefan, Silvia Ienciu, Octavian Marius Cretu, Roxana Popescu, Cristina Gluhovschi, Lavinia Iancu and Adrian Vlad
Biomolecules 2024, 14(4), 499; https://doi.org/10.3390/biom14040499 - 19 Apr 2024
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Abstract
Cerebrovascular disease accounts for major neurologic disabilities in patients with type 2 diabetes mellitus (DM). A potential association of mitochondrial DNA (mtDNA) and inflammation with cerebral vessel remodeling in patients with type 2 DM was evaluated. A cohort of 150 patients [...] Read more.
Cerebrovascular disease accounts for major neurologic disabilities in patients with type 2 diabetes mellitus (DM). A potential association of mitochondrial DNA (mtDNA) and inflammation with cerebral vessel remodeling in patients with type 2 DM was evaluated. A cohort of 150 patients and 30 healthy controls were assessed concerning urinary albumin/creatinine ratio (UACR), synaptopodin, podocalyxin, kidney injury molecule-1 (KIM-1), N-acetyl-β-(D)-glucosaminidase (NAG), interleukins IL-17A, IL-18, IL-10, tumor necrosis factor-alpha (TNFα), intercellular adhesion molecule-1 (ICAM-1). MtDNA-CN and nuclear DNA (nDNA) were quantified in peripheral blood and urine by qRT-PCR. Cytochrome b (CYTB) gene, subunit 2 of NADH dehydrogenase (ND2), and beta 2 microglobulin nuclear gene (B2M) were assessed by TaqMan assays. mtDNA-CN was defined as the ratio of the number of mtDNA/nDNA copies, through analysis of the CYTB/B2M and ND2/B2M ratio; cerebral Doppler ultrasound: intima-media thickness (IMT)—the common carotid arteries (CCAs), the pulsatility index (PI) and resistivity index (RI)- the internal carotid arteries (ICAs) and middle cerebral arteries (MCAs), the breath-holding index (BHI). The results showed direct correlations of CCAs-IMT, PI-ICAs, PI-MCAs, RI-ICAs, RI-MCAs with urinary mtDNA, IL-17A, IL-18, TNFα, ICAM-1, UACR, synaptopodin, podocalyxin, KIM-1, NAG, and indirect correlations with serum mtDNA, IL-10. BHI correlated directly with serum IL-10, and serum mtDNA, and negatively with serum IL-17A, serum ICAM-1, and NAG. In neurologically asymptomatic patients with type 2 DM cerebrovascular remodeling and impaired cerebrovascular reactivity may be associated with mtDNA variations and inflammation from the early stages of diabetic kidney disease. Full article
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