Mitoprotective Clinical Strategies in Type 2 Diabetes and Fanconi Anemia Patients: Suggestions for Clinical Management of Mitochondrial Dysfunction
| Autor: | Maria Rosa Fittipaldi, Beatriz Porto, Marco Trifuoggi, Giovanni Pagano, Alex Lyakhovich, Federico V. Pallardó |
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| Přispěvatelé: | Pagano, G., Pallardo, F. V., Porto, B., Fittipaldi, M. R., Lyakhovich, A., Trifuoggi, M. |
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Physiology medicine.medical_treatment Clinical Biochemistry mitochondrial nutrients Disease Type 2 diabetes Review Bioinformatics medicine.disease_cause Biochemistry 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine In vivo Fanconi anemia mitochondrial dysfunction medicine oxidative stress Molecular Biology fanconi anemia Coenzyme Q10 business.industry lcsh:RM1-950 Mitochondrial nutrient Cell Biology medicine.disease Phenotype 030104 developmental biology lcsh:Therapeutics. Pharmacology chemistry 030220 oncology & carcinogenesis Oxidative stre type 2 diabetes business Adjuvant Oxidative stress |
| Zdroj: | Antioxidants, Vol 9, Iss 1, p 82 (2020) Antioxidants |
| ISSN: | 2076-3921 |
| Popis: | Oxidative stress (OS) and mitochondrial dysfunction (MDF) occur in a number of disorders, and several clinical studies have attempted to counteract OS and MDF by providing adjuvant treatments against disease progression. The present review is aimed at focusing on two apparently distant diseases, namely type 2 diabetes (T2D) and a rare genetic disease, Fanconi anemia (FA). The pathogenetic links between T2D and FA include the high T2D prevalence among FA patients and the recognized evidence for OS and MDF in both disorders. This latter phenotypic/pathogenetic feature—namely MDF—may be regarded as a mechanistic ground both accounting for the clinical outcomes in both diseases, and as a premise to clinical studies aimed at counteracting MDF. In the case for T2D, the working hypothesis is raised of evaluating any in vivo decrease of mitochondrial cofactors, or mitochondrial nutrients (MNs) such as α-lipoic acid, coenzyme Q10, and l-carnitine, with possibly combined MN-based treatments. As for FA, the established knowledge of MDF, as yet only obtained from in vitro or molecular studies, prompts the requirement to ascertain in vivo MDF, and to design clinical studies aimed at utilizing MNs toward mitigating or delaying FA’s clinical progression. Altogether, this paper may contribute to building hypotheses for clinical studies in a number of OS/MDF-related diseases. |
| Databáze: | OpenAIRE |
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