Chemotherapy remodels lung adenocarcinoma’s tumor microenvironment by driving metabolic reprogramming and shifting immune cell functions to modulate tumor progression and immune responses.

Single-cell RNA sequencing reveals Nrg1/ErbB2-induced metabolic reprogramming as a pivotal event for cardiomyocyte proliferation during heart regeneration.

Single-cell expression profiling and genetic lineage analysis show that aging impairs adipocyte differentiation from precursor cells and blocks the thermogenic activation of adipocytes during cold exposure.

Genetic analyses and biochemical studies show that JMJD6 promotes MYC-mediated transformation and is required for neuroblastoma growth by complexing with pre-mRNA splicing factors.

Pathological TNF-α-producing B cells are involved in the pathological process of polycystic ovary syndrome, and metformin inhibits mTOR phosphorylation, affects metabolic reprogramming, and further inhibits TNF-α expression in pathological B cells.

ATF4, the master regulator of transcription during the Integrated Stress Response (ISR), causes global changes in cysteine sulfhydration of proteins and this event causes cellular metabolic reprogramming.

Hemodynamic forces regulate endothelial cell metabolism, which in turn regulates endothelial inflammation.

A non-canonical p53 function in adipocyte plays a critical role in energy homeostasis and is involved in obesity-associated metabolic dysfunctions.

A novel role of the mitochondrial BK_Ca channel involves the metabolic reprogramming of breast cancer cells, facilitating their unrestricted proliferation and O₂-independence, which is also of potential clinical relevance.

Gene knockout in cell lines and mice reveal that store-operated calcium entry is synergistically mediated by Orai1 and Orai3 channel proteins in B cells and is important for signaling to the nucleus and metabolic activity in response to antigenic stimulation.