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Metabolic Reprogramming in Health and Disease 2.0

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

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 2784

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Department of Surgical Pathology, Università di Pisa, 56126 Pisa, Italy
Interests: metabolic biochemistry; thyroid hormone analogs and metabolites; vitamin D analogs; drug design, synthesis and development
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Special Issue Information

Dear Colleagues,

Metabolism is broadly defined as the sum of biochemical processes in living organisms that either produce or consume energy.

It is widely acknowledged that metabolic perturbations, often genetically programmed, accompany common human diseases. Among these, cancer is a prime example of a disease with genetically defined, pathological metabolic perturbations. Indeed, metabolic reprogramming, such as enhanced aerobic glycolysis, mutations in the tricarboxylic acid (TCA) cycle metabolic enzymes, and dependence on lipid and glutamine metabolism are key characteristics of cancer cells. Therefore, addressing such metabolic perturbations is a very promising direction for anti-cancer therapies that, in combination with conventional chemotherapeutic agents, may enhance therapeutic efficacy and clinical outcomes.

One of the main challenges in human metabolism research is to analyze the impact of disease on metabolic flux in vivo by relying on the use of sensitive and efficient methods, such as NMR spectroscopy or mass spectrometry techniques, in order to measure the transfer of carbon, nitrogen, etc., in metabolic pathways of live subjects, with and without disease. These approaches are becoming increasingly used and will likely find key applications in understanding the metabolic basis of common human diseases, paving the way for the translation of this knowledge into novel diagnostic and therapeutic approaches.

This Special Issue of the International Journal of Molecular Sciences, “Metabolic Reprogramming in Health and Disease 2.0”, will focus on the broad impact of metabolism in cellular function, and how modern concepts of metabolism can inform our understanding of common diseases, including cancer, obesity, diabetes and neurodegenerative disorders, and considers the prospects of developing new metabolic approaches to disease treatment.

Authors are invited to contribute a full original research paper or review article for peer-review and publication.

Prof. Dr. Grazia Chiellini
Guest Editor

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Published Papers (1 paper)

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26 pages, 1258 KiB  
Review
Evolutionary Origins of Metabolic Reprogramming in Cancer
by Natalia García-Sancha, Roberto Corchado-Cobos, Aurora Gómez-Vecino, Alejandro Jiménez-Navas, Manuel Jesús Pérez-Baena, Adrián Blanco-Gómez, Marina Holgado-Madruga, Jian-Hua Mao, Javier Cañueto, Sonia Castillo-Lluva, Marina Mendiburu-Eliçabe and Jesús Pérez-Losada
Int. J. Mol. Sci. 2022, 23(20), 12063; https://doi.org/10.3390/ijms232012063 - 11 Oct 2022
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Abstract
Metabolic changes that facilitate tumor growth are one of the hallmarks of cancer. These changes are not specific to tumors but also take place during the physiological growth of tissues. Indeed, the cellular and tissue mechanisms present in the tumor have their physiological [...] Read more.
Metabolic changes that facilitate tumor growth are one of the hallmarks of cancer. These changes are not specific to tumors but also take place during the physiological growth of tissues. Indeed, the cellular and tissue mechanisms present in the tumor have their physiological counterpart in the repair of tissue lesions and wound healing. These molecular mechanisms have been acquired during metazoan evolution, first to eliminate the infection of the tissue injury, then to enter an effective regenerative phase. Cancer itself could be considered a phenomenon of antagonistic pleiotropy of the genes involved in effective tissue repair. Cancer and tissue repair are complex traits that share many intermediate phenotypes at the molecular, cellular, and tissue levels, and all of these are integrated within a Systems Biology structure. Complex traits are influenced by a multitude of common genes, each with a weak effect. This polygenic component of complex traits is mainly unknown and so makes up part of the missing heritability. Here, we try to integrate these different perspectives from the point of view of the metabolic changes observed in cancer. Full article
(This article belongs to the Special Issue Metabolic Reprogramming in Health and Disease 2.0)
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