Metabolic dysregulation in myelodysplastic neoplasm: impact on pathogenesis and potential therapeutic targets.

Autor: Zhou H; Department of Hematology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China., Xiang W; Department of Hematology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China., Zhou G; Department of Hematology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China., Rodrigues-Lima F; Université Paris Cité, CNRS, Unité de Biologie Fonctionnelle Et Adaptative, 75013, Paris, France., Guidez F; Université Paris Cité, Institut de Recherche Saint Louis INSERM UMR_S1131, 75010, Paris, France., Wang L; Department of Hematology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China. liwang@hospital.cqmu.edu.cn.
Jazyk: angličtina
Zdroj: Medical oncology (Northwood, London, England) [Med Oncol] 2024 Dec 07; Vol. 42 (1), pp. 23. Date of Electronic Publication: 2024 Dec 07.
DOI: 10.1007/s12032-024-02575-3
Abstrakt: Despite significant advancements in the research of the pathogenesis mechanisms of Myelodysplastic Neoplasm (MDS) in recent years, there are still many gaps to fill. The advancement of metabolomics studies has led to a research booming in clarifying the impact of metabolic abnormalities during the pathogenesis of MDS. The present review primarily focuses on the dysregulated metabolic pathways, exploring the influences on the pathogenesis of MDS and their roles during the course of the disease. Furthermore, we discuss the potential of relevant metabolic pathways as therapeutic targets, along with the latest metabolic-related treatment drugs and approaches.
Competing Interests: Declarations. Competing Interests: The authors declare no competing interests.
(© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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