Innovative strategies for mitochondrial dysfunction in myeloproliferative neoplasms a step toward precision medicine

Sep 3, 2025Annals of medicine and surgery (2012)

New approaches to fixing energy problems in blood cancers for personalized treatment

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Abstract

is associated with increased reactive oxygen species production and apoptosis resistance in myeloproliferative neoplasms (MPNs).

Mutations in JAK2, CALR, and myeloproliferative leukemia are primarily responsible for the constitutive activation of the JAK-STAT pathway in MPNs.
Mitochondrial dysfunction contributes to clonal expansion in MPNs through increased reactive oxygen species and mitochondrial DNA mutations.
Targeting mitochondrial pathways may offer therapeutic strategies, including mitochondria-targeted antioxidants and metabolic inhibitors.
Challenges such as drug delivery specificity and therapeutic resistance need to be addressed in developing treatments for MPNs.
Advances in could allow for tailored interventions based on individual mutation patterns in MPN patients.

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Myeloproliferative neoplasms (MPNs) are clonal disorders of hematopoietic stem cells characterized by aberrant proliferation of myeloid lineages, driven primarily by mutations in JAK2, CALR, and myeloproliferative leukemia, leading to constitutive activation of the JAK-STAT pathway. Emerging evidence highlights as a key factor in MPN pathogenesis, contributing to increased reactive oxygen species production, mitochondrial DNA mutations, and dysregulated mitochondrial dynamics, which collectively promote clonal expansion and apoptosis resistance. Targeting mitochondrial pathways has gained attention as a therapeutic strategy, with approaches including mitochondria-targeted antioxidants, metabolic inhibitors, and modulation of mitophagy and mitochondrial fission/fusion dynamics. However, challenges such as drug delivery specificity, therapeutic resistance, and off-target effects remain significant. Recent advances in , incorporating genomic, transcriptomic, and proteomic profiling, offer a more personalized approach to MPN treatment by tailoring interventions to individual mutation patterns. Additionally, novel therapeutic strategies, including gene editing technologies, RNA-based therapies, and nanoparticle-mediated drug delivery systems, hold promise for overcoming current treatment limitations. The integration of artificial intelligence in drug discovery and biomarker identification further enhances the potential for targeted therapies. Future research should focus on refining these strategies, developing reliable biomarkers for patient stratification, and exploring combination therapies that enhance treatment efficacy while minimizing adverse effects. By addressing mitochondrial dysfunction as an underlying driver of MPNs, these emerging approaches have the potential to improve disease management, extend patient survival, and enhance quality of life. Also, this new approach of precision medicine allows patient stratification and ensures that treatments are formed according to the individual disease biology of each patient, which results in overall better outcomes.

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Innovative strategies for mitochondrial dysfunction in myeloproliferative neoplasms a step toward precision medicine

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