
This study reveals that TGF-β-induced myofibroblast activation relies on the metabolic maladaptation of the solute carrier SLC1A5, responsible for cellular glutamine uptake. Fibrotic lung fibroblasts and those from idiopathic pulmonary fibrosis lungs exhibit heightened SLC1A5 expression. Inhibiting SLC1A5 disrupts fibroblast activation, impacting autophagy, mTOR, HIF, Myc signaling, and cellular energetics.
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