[Research Progress of Mitochondrial Dynamics in Leukemia --Review].

Mitochondria is one of the most important organelles of eukaryotic cells, which is closely related to cell proliferation, apoptosis, autophagy and other life processes. Mitochondrias in biological cells are actually in a highly dynamic state. The fusion and division of mitochondria and their secondary effects play an important role in the regulation of cell life. As a malignant disease of hematopoietic system, leukemia is characterized by excessive proliferation, limited apoptosis, abnormal autophagy and other abnormal cell regulation. Therefore, abnormal mitochondrial dynamics regulation may play a key role in the pathogenesis of leukemia, refractory and drug resistance of leukemia. The article reviews the role of mitochondrial dynamics and abnormal regulation in the pathogenesis and development of leukemia, and provides a theoretical basis for the research on the regulation of mitochondrial dynamics in leukemia.

Genome-wide identification of aberrant alternative splicing and RNA-binding protein regulators in acute myeloid leukaemia which may contribute to immune microenvironment remodelling.

Acute myeloid leukaemia (AML) is one of the most lethal cancers of the haematopoietic system with a poorly understood aetiology. Recent studies have shown that aberrant alternative splicing (AS) and a (RBP) regulators are highly associated with the pathogenesis of AML. This study presents an overview of the abnormal AS and differential expression of RNA-binding proteins (RBPs) in AML and further highlights their close relation to the remodelling of the immune microenvironment in AML patients. An in-depth understanding of the regulatory mechanism underlying AML will contribute to the future development of strategies for the prevention, diagnosis and therapy of AML and thus improve the overall survival of patients with AML.

Role of heteroplasmic mutations in the mitochondrial genome and the ID4 gene promoter methylation region in the pathogenesis of chronic aplastic anemia in patients suffering from Kidney yin deficiency.

OBJECTIVE: To analyze changes in gene amplification in the mitochondrial genome and in the ID4 gene promoter methylation region in patients with chronic aplastic anemia (CAA) suffering from Kidney (Shen) yin deficiency or Kidney yang deficiency. METHODS: Bone marrow and oral epithelium samples were collected from CAA patients with Kidney yin deficiency or Kidney yang deficiency (20 cases). Bone marrow samples were collected from 20 healthy volunteers. The mitochondrial genome was amplified by polymerase chain reaction (PCR), and PCR products were used for sequencing and analysis. RESULTS: Higher mutational rates were observed in the ND1-2, ND4-6, and CYTB genes in CAA patients suffering from Kidney yin deficiency. Moreover, the ID4 gene was unmethylated in bone marrow samples from healthy individuals, but was methylated in some CAA patients suffering from Kidney yin deficiency (positive rate, 60%) and Kidney yang deficiency (positive rate, 55%). CONCLUSIONS: These data supported that gene mutations can alter the expression of respiratory chain enzyme complexes in CAA patients, resulting in energy metabolism impairment and promoting the physiological and pathological processes of hematopoietic failure. Functional impairment of the mitochondrial respiration chain induced by gene mutation may be an important reason for hematopoietic failure in patients with CAA. This change is closely related to maternal inheritance and Kidney yin deficiency. Finally, these data supported the assertion that it is easy to treat disease in patients suffering from yang deficiency and difficult to treat disease in patients suffering from yin deficiency.