Myofibroblasts and Fibrosis: Mitochondrial and Metabolic Control of Cellular Differentiation.

Circulation Research
Andrew A GibbJohn W Elrod

Abstract

Cardiac fibrosis is mediated by the activation of resident cardiac fibroblasts, which differentiate into myofibroblasts in response to injury or stress. Although myofibroblast formation is a physiological response to acute injury, such as myocardial infarction, myofibroblast persistence, as occurs in heart failure, contributes to maladaptive remodeling and progressive functional decline. Although traditional pathways of activation, such as TGFβ (transforming growth factor β) and AngII (angiotensin II), have been well characterized, less understood are the alterations in mitochondrial function and cellular metabolism that are necessary to initiate and sustain myofibroblast formation and function. In this review, we highlight recent reports detailing the mitochondrial and metabolic mechanisms that contribute to myofibroblast differentiation, persistence, and function with the hope of identifying novel therapeutic targets to treat, and potentially reverse, tissue organ fibrosis.

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Citations

Jan 1, 2021·Biochimica Et Biophysica Acta. Molecular Basis of Disease·Nicola ChiarelliMarina Colombi
Feb 12, 2021·Nature Reviews. Cardiology·Begoña LópezJavier Díez
May 15, 2021·Clinical Science·Abdul Waheed KhanKarin A M Jandeleit-Dahm
May 16, 2021·Acta Pharmacologica Sinica·Yuan-Yuan ChenSen Zhang
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Jun 13, 2021·Wound Repair and Regeneration : Official Publication of the Wound Healing Society [and] the European Tissue Repair Society·Wolfgang MerktDavid Lagares
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Aug 9, 2021·The Journal of Biological Chemistry·Emma L WoodsRobert Steadman
Apr 18, 2021·Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine·Gyu Seong HeoYongjian Liu

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