Hu-Hu Zhang

Mcu upregulation triggers mitochondrial oxidative stress and cardiomyocyte injury after myocardial infarction yet is suppressed by Fto and Ythdf2 in an m6A-dependent manner.

It is demonstrated that elevated Mcu is positively associated with MI risk; excess Mcu triggers mitochondrial calcium overload, ROS buildup, mitochondrial membrane potential loss and respiratory chain damage to facilitate cardiomyocyte damage, whereas Mcu knockdown alleviate these pathological alterations.

RBM protein family: Focusing on the occurrence, progression and treatment of cancer

BMSC-derived EVs alleviate doxorubicin-induced cardiotoxicity via miR-210-3p involving the ACVR1B-SMAD3-PGC-1α signaling axis

Doxorubicin-induced cardiotoxicity (DIC) limits the clinical use of doxorubicin, yet no specific therapeutic interventions are available. Although the cardioprotective role of miR-210 and the therapeutic potential of stem cell-derived extracellular vesicles have been reported, the specific downstream effectors and path...

FABPs-mediated lipid signaling pathways in tumor reprogramming: bidirectional crosstalk with the immune microenvironment.

Fatty acid-binding proteins (FABPs) are cytoplasmic lipid chaperones that regulate intracellular fatty acid trafficking and metabolic homeostasis. Increasing evidence identifies FABPs as key drivers of tumor metabolic reprogramming. Within the broader tumor microenvironment (TME), particularly its immune compartment, t...