Cardiac fibroblast and myofibroblast  

Fibroblasts are interstitial mesenchymallike cells and highly heterogeneous,remain poorly defined. Cardiomyocytes occupy about 75% volume, whereas

cardiac fibroblasts are found throughout cardiac tissue and occupy12/3 cell numbers in the adult heart.They are embedded in extracellular matrix of connective tissue(collagenand fibronectin).CM form collagen type IV as part of theirbasement membrane, while CF product collagen I, III and VI. CFs vary widely with location and metabolic activity, containing an oval nucleus, extensive rough ER, a prominent Golgi apparatus and abundant cytoplasmic graular material. A useful label for CFs are vimentin that react with the abundantintermediate filaments of fibroblasts.Fibroblasts interact with their surrounding microenvironment through alpha/beta integrin.Typically, fibroblasts are fusiform cells with intermediate filaments. Once activated, fibroblasts own heterotypic change and secrete increasingly ECM. Alpha-smooth-actin stress actin character CFs.

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The ECM and growth factor secreted from CFs are essential for cardiac remodeling.CFs constitute the mesenchymal component and possess complex sources and function(smooth muscle actin, vimentin,collagen,S100A4, CD90,PDGFRa).During development, most CFs are of epicardial origin(80%) and 16% are endocardial（undergoing epithelialtomesenchymal transitionEMT）.

  Cardiac myofibroblasts are found in pressure overload owing to myocardial infarction, hypertension, inflammation, and other stress signals. CMFs are absent from normal heart (except for heart valve), but they participate in cardiac wound and repair. And CMFs are actived in cardiac remodeling and fibrotic scar.Myofibroblasts exhibit a contractile cell phenotype intermediate between that of fibroblasts and smooth muscle cells. Compared with CFs, CMFs are are larger cells with increased expression of stress fibers that exhibit enhanced proliferation, migration, and secretion of ECM proteins, ECM degradation enzymes and their inhibitors.In addition, microfibroblasts show both the increased secretion of and responsiveness to various cytokines and growth factors.  

  While during pressure overload induced cardiac lesions, CFs are derived from endothelium, bone marrow and blood.The strongest signatureof CF cells was

gata4 and tbx20. CF to CM conversion has been successfully reprogramed in mouse and human.CFs are the main curse of fibrosis. Fibrosis causes exacerbated collagen deposition, which increases myocardial stiffness.Scars are capables of generating arrhythmias.

References:

1.View from the heart: cardiac fibroblasts in development, scarring and regeneration

2.Fibroblasts in cancer

3.Cardiac Fibroblasts Regulate Myocardial Proliferation through b1 Integrin Signaling

4.Cardiac Fibroblasts and Arrhythmogenesis

5.Structural and functional characterisation of cardiacfibroblasts

6.Redefining the identity of cardiac fibroblasts