Autophagy is a catabolic pathway essential for cellular energy homeostasis that involves the self-degradation of intracellular components in lysosomes. This process has been implicated in the pathophysiology of many human disorders, including infection, cancer, and fibrosis. Autophagy is also recognized as a mediator of survival and proliferation, and multiple pathways induce autophagy under conditions of cellular stress, including nutrient and energy depletion. High autophagic activity has been detected in fibrogenic cells from several tissues; however the role of autophagy in fibrogenesis and mesenchymal cells varies greatly in different tissues and settings, with contributions uncovered to energy metabolism and collagen turnover by fibrogenic cells. Because several chemical modulators of autophagy have already been identified, autophagy regulation constitutes a potential target for antifibrotic therapy. This article is part of a Special Issue entitled: Fibrosis: Translation of basic research to human disease.

Original languageEnglish
Pages (from-to)972-978
Number of pages7
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Issue number7
StatePublished - Jul 2013


  • Energy homeostasis
  • Fibroblast and fibrotic diseases
  • Fibrosis
  • Mesenchymal cells


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