TY - JOUR
T1 - State of change
T2 - epigenetic and mitochondrial regulation of cardiac fibroblast activation
AU - Garvin, Alexandra M.
AU - Hale, Taben M.
N1 - Publisher Copyright:
© 2022 Elsevier Ltd
PY - 2022/8
Y1 - 2022/8
N2 - Cardiac fibroblasts (CFs) exist in a variety of states that contribute to either conserved or uncontrolled extracellular matrix (ECM) deposition. In healthy hearts, fibroblasts favor the homeostatic or quiescent state in which they work to maintain the ECM at a baseline level of activity. Acute or chronic injury in the form of myocardial infarction, hypertension, and heart failure induce CF activation via increased pro-oxidant, proinflammatory, and profibrotic stimuli secondary to hypoxia, cardiomyocyte cell death, or hemodynamic stress. In addition to the well-described signaling molecules that induce CF activation (e.g. transforming growth factor beta 1, angiotensin II, and reactive oxygen species), there are emerging concepts that describe mechanisms that regulate more nuanced transition between activation states. This review will discuss recent descriptions of heterogeneous populations of resident cardiac fibroblasts, states of fibroblast activation, and the roles for mitochondrial and chromatin accessibility in mediating transition to and persistence of the activated state.
AB - Cardiac fibroblasts (CFs) exist in a variety of states that contribute to either conserved or uncontrolled extracellular matrix (ECM) deposition. In healthy hearts, fibroblasts favor the homeostatic or quiescent state in which they work to maintain the ECM at a baseline level of activity. Acute or chronic injury in the form of myocardial infarction, hypertension, and heart failure induce CF activation via increased pro-oxidant, proinflammatory, and profibrotic stimuli secondary to hypoxia, cardiomyocyte cell death, or hemodynamic stress. In addition to the well-described signaling molecules that induce CF activation (e.g. transforming growth factor beta 1, angiotensin II, and reactive oxygen species), there are emerging concepts that describe mechanisms that regulate more nuanced transition between activation states. This review will discuss recent descriptions of heterogeneous populations of resident cardiac fibroblasts, states of fibroblast activation, and the roles for mitochondrial and chromatin accessibility in mediating transition to and persistence of the activated state.
KW - Cardiac fibroblast
KW - Epigenetics
KW - Heart
KW - Mitochondria
KW - Myofibroblas
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U2 - 10.1016/j.cophys.2022.100557
DO - 10.1016/j.cophys.2022.100557
M3 - Review article
AN - SCOPUS:85133717392
SN - 2468-8681
VL - 28
JO - Current Opinion in Physiology
JF - Current Opinion in Physiology
M1 - 100557
ER -