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Targeting Metabolic Reprogramming: From Pathogenesis to Therapeutic Strategies

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: 20 May 2025 | Viewed by 673

Special Issue Editors


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Guest Editor
Departamento Fisiologia Humana, Histologia Humana, Anatomia Patologica y Educacion Fisica y Deportiva, Facultad de Medicina, Universidad de Malaga, 29071 Malaga, Spain
Interests: myelin; oligodendrocyte; neurodegenerative disease; metabolism

E-Mail Website
Guest Editor
Departamento Fisiologia Humana, Histologia Humana, Anatomia Patologica y Educacion Fisica y Deportiva, Facultad de Medicina, Universidad de Malaga, 29071 Malaga, Spain
Interests: immunopathology; oncology; haemathology; autoinmune diseases

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Guest Editor
Departamento Fisiologia Humana, Histologia Humana, Anatomia Patologica y Educacion Fisica y Deportiva, Facultad de Medicina, Universidad de Malaga, 29071 Malaga, Spain
Interests: Alzheimer’s disease; transgenic models; neuroinflammation; tauopathy
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Special Issue Information

Dear Colleagues,

Metabolic reprogramming is a hallmark of cancer cells, but it also occurs in other pathological conditions such as chronic lung diseases, rheumatoid arthritis, cardiovascular diseases, neurodegenerative diseases, and viral pathogenesis, among others.

Despite the increasing interest in this field, the molecular mechanisms underlying metabolic reprogramming in many of the above-mentioned pathologies are still scarce. Metabolic reprogramming might involve changes in glycolysis, the pentose phosphate pathway, glutaminolysis, mitochondrial metabolism, lipid metabolism, amino acid metabolism, or any other biosynthetic and bioenergetic pathways. Therefore, any natural or synthetic compound capable of modifying the activity of any of these pathways altered in the aforementioned diseases might be considered a potential therapeutic candidate to test.

This Special Issue aims to gather a broad collection of any basic and preclinical research that investigates metabolic reprogramming as a key regulator in diverse disease pathogenesis and as a novel target to decipher innovative therapeutic strategies.

Dr. Beatriz García-Díaz
Prof. Dr. Alejandro Escamilla
Prof. Dr. Raquel Sanchez-Varo
Guest Editors

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Keywords

  • metabolism
  • therapy
  • mitochondria
  • pathogenesis
  • bioenergetics

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Published Papers (1 paper)

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Research

15 pages, 13508 KiB  
Article
Distinct Hepatic Metabolic Reprogramming in Acute and Chronic Sleep Deprivation and the Protective Effects of the Chalcone Analogue TAK
by Yifang Wang, Yachong Hu, Pengxiao Wang, Ranrui Hu, Zhongqi Chen, Tiantian Zhang, Jiankang Liu, Mami Noda, Jiangang Long and Yunhua Peng
Int. J. Mol. Sci. 2025, 26(8), 3485; https://doi.org/10.3390/ijms26083485 - 8 Apr 2025
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Abstract
The prevalence of sleep deprivation is increasing worldwide. Despite the vital roles that the liver plays in metabolism and immune response, hepatic dysfunctions in acute sleep deprivation (ASD) and chronic sleep deprivation (CSD) remain underexplored. Additionally, the effects of the newly developed chalcone [...] Read more.
The prevalence of sleep deprivation is increasing worldwide. Despite the vital roles that the liver plays in metabolism and immune response, hepatic dysfunctions in acute sleep deprivation (ASD) and chronic sleep deprivation (CSD) remain underexplored. Additionally, the effects of the newly developed chalcone analog, 1-(2,3,4-trimethoxyphenyl)-2-(3,4,5-trimethoxyphenyl)-acrylketone (TAK), were evaluated as a potential therapeutic chemical for mitigating SD-induced hepatic damage. A modified multi-platform method was employed to prepare animal models of 72 h ASD and 21-day CSD in rats. TAK (50 mg/kg/day) was administered through irrigation starting one week before the experiment and continuing until the end. ASD triggered hepatic lipid accumulation and inflammation, whereas CSD resulted in pathological portal area expansion and fibrosis, with comparatively fewer disturbances in liver metabolism and inflammation. TAK effectively alleviated ASD-induced disruptions in glycogen synthesis via PI3K/AKT/GSK3/GYS2 pathways, abnormal lipid accumulation via SREBP1/FASN/ACC, liver inflammation by balancing M1 and M2 macrophages, and liver fibrosis induced by ASD/CSD. This study provides valuable insights into the different mechanisms of liver damage induced by severe ASD and mild CSD. Additionally, TAK has been proposed as a potential therapeutic strategy for ultimate SD-related hepatic complications. Full article
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