Role of mitochondrial structural and functional alterations in bcl-2 inhibitor resistance in acute myeloid leukemia
10.3760/cma.j.cn115356-20230714-00146
- VernacularTitle:线粒体结构及功能改变在急性髓系白血病bcl-2抑制剂耐药中的作用
- Author:
Xiaorui WANG
1
;
Qian WANG
Author Information
1. 复旦大学附属华山医院血液科，上海 200040
- Keywords:
Leukemia, myeloid, acute;
Mitochondria;
Genes, bcl-2;
Venetoclax;
Drug resistance
- From:
Journal of Leukemia & Lymphoma
2024;33(8):494-497
- CountryChina
- Language:Chinese
-
Abstract:
For patients suffering from relapsed/refractory acute myeloid leukemia, particularly among the elderly patients, the utilization of bcl-2 inhibitors, represented by venetoclax (ABT199), has demonstrated a notable initial response rate either as a standalone therapy or when combined with other demethylating agents. However, drug resistance also occurs, and the mechanism is unclear. Bcl-2 inhibitors primarily exert their effects on intracellular mitochondria. Alterations in mitochondrial function and structure are involved in multiple pathologic processes contributing to the development of bcl-2 inhibitor resistance, such as oxidative phosphorylation, lipid metabolism, amino acid metabolism and mitochondrial-mediated cell death. This review will describe the role of mitochondrial structural and functional alterations in bcl-2 inhibitor resistance in acute myeloid leukemia.
