Lung tissue glycolysis metabolism

Lung tissue glycolysis metabolism refers to the enzymatic breakdown of glucose within pulmonary cells to generate ATP and biosynthetic intermediates. In healthy lung tissue, energy is primarily derived from oxidative phosphorylation, but pathological states often trigger a shift toward aerobic glycolysis, known as the Warburg effect [PubMed: 27079511]. This metabolic reprogramming is a hallmark of lung cancer, where it supports the high energy demands of rapidly dividing cells and contributes to therapeutic resistance [NIH: PMC4783224]. Beyond oncology, increased glycolytic activity is observed in idiopathic pulmonary fibrosis (IPF), where it promotes fibroblast-to-myofibroblast differentiation and extracellular matrix production [PubMed: 28615295]. In pulmonary arterial hypertension (PAH), glycolytic shifts in the pulmonary vasculature drive cell proliferation and suppress apoptosis, leading to vascular remodeling [PubMed: 18463671]. While the pathway itself is not a single molecular target, specific components such as Hexokinase 2 (HK2) and PFKFB3 are targeted by experimental agents like 2-deoxy-D-glucose and PFK158 to treat these conditions [PubMed: 30217977]. Clinical monitoring of this pathway often employs 18F-fluorodeoxyglucose (FDG) PET imaging as a biomarker for disease severity and metabolic activity [StatPearls: NBK538236].

Other names

Pulmonary glycolysisLung glucose metabolismAerobic glycolysis in lung tissueWarburg effect in lung

Inhibition of rate-limiting glycolytic enzymes to disrupt energy production and biosynthetic pathways in hyper-metabolic diseased cells.