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Redefining the identity of cardiac fibroblasts

Key Points

  • Cardiac fibroblasts are critical regulators of the basal structure of the heart and are also responsible for remodelling and fibrosis after injury

  • The identity and origin of disease-activated fibroblasts within the heart has been an ongoing debate

  • Tissue-resident fibroblasts of embryonic origin are interspersed throughout the adult mouse heart and comprise 10% of the total cell content

  • Recent studies indicate that tissue-resident fibroblasts differentiate into and constitute the majority of disease-activated fibroblasts and myofibroblasts after cardiac injury

  • Activated fibroblasts or myofibroblasts within the injured mouse heart are not appreciably derived from other non-tissue-resident fibroblast cell sources

Abstract

Cardiac fibroblasts deposit and maintain extracellular matrix during organogenesis and under physiological conditions. In the adult heart, activated cardiac fibroblasts also participate in the healing response after acute myocardial infarction and during chronic disease states characterized by augmented interstitial fibrosis and ventricular remodelling. However, delineation of the characteristics, plasticity, and origins of cardiac fibroblasts is an area of ongoing investigation and controversy. A set of genetic mouse models has been developed that specifically addresses the nature of these cells, in terms of both their origins and their response during cardiac disease and ventricular remodelling. As our understanding of cardiac fibroblasts becomes more defined and refined, so does the potential to develop new therapeutic strategies to control fibrosis and adverse ventricular remodelling.

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Figure 1: Current categories of resident cardiac fibroblasts.
Figure 2: Developmental and alternative sources of fibroblasts.
Figure 3: Lineage tracing of resident cardiac fibroblasts.

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References

  1. Mozaffarian, D. et al. Heart disease and stroke statistics — 2015 update: a report from the American Heart Association. Circulation 131, e29–e322 (2015).

    PubMed  Google Scholar 

  2. Gourdie, R. G., Dimmeler, S. & Kohl, P. Novel therapeutic strategies targeting fibroblasts and fibrosis in heart disease. Nat. Rev. Drug Discov. 15, 620–638 (2016).

    CAS  PubMed  PubMed Central  Google Scholar 

  3. Shinde, A. V. & Frangogiannis, N. G. Fibroblasts in myocardial infarction: a role in inflammation and repair. J. Mol. Cell. Cardiol. 70, 74–82 (2014).

    CAS  PubMed  Google Scholar 

  4. Davis, J. & Molkentin, J. D. Myofibroblasts: trust your heart and let fate decide. J. Mol. Cell. Cardiol. 70, 9–18 (2014).

    CAS  PubMed  Google Scholar 

  5. Borthwick, L. A., Wynn, T. A. & Fisher, A. J. Cytokine mediated tissue fibrosis. Biochim. Biophys. Acta 1832, 1049–1060 (2013).

    CAS  PubMed  Google Scholar 

  6. Porter, K. E. & Turner, N. A. Cardiac fibroblasts: at the heart of myocardial remodeling. Pharmacol. Ther. 123, 255–278 (2009).

    CAS  PubMed  Google Scholar 

  7. Liu, T. et al. Lack of MK2 inhibits myofibroblast formation and exacerbates pulmonary fibrosis. Am. J. Respir. Cell Mol. Biol. 37, 507–517 (2007).

    CAS  PubMed  PubMed Central  Google Scholar 

  8. Swonger, J. M., Liu, J. S., Ivey, M. J. & Tallquist, M. D. Genetic tools for identifying and manipulating fibroblasts in the mouse. Differentiation 92, 66–83 (2016).

    CAS  PubMed  PubMed Central  Google Scholar 

  9. Moore-Morris, T., Guimaraes-Camboa, N., Yutzey, K. E., Puceat, M. & Evans, S. M. Cardiac fibroblasts: from development to heart failure. J. Mol. Med. (Berl.) 93, 823–830 (2015).

    CAS  Google Scholar 

  10. Moore-Morris, T. et al. Resident fibroblast lineages mediate pressure overload-induced cardiac fibrosis. J. Clin. Invest. 124, 2921–2934 (2014).

    CAS  PubMed  PubMed Central  Google Scholar 

  11. Kanisicak, O. et al. Genetic lineage tracing defines myofibroblast origin and function in the injured heart. Nat. Commun. 7, 12260 (2016).

    CAS  PubMed  PubMed Central  Google Scholar 

  12. Ali, S. R. et al. Developmental heterogeneity of cardiac fibroblasts does not predict pathological proliferation and activation. Circ. Res. 115, 625–635 (2014).

    CAS  PubMed  Google Scholar 

  13. Weber, K. T., Sun, Y., Bhattacharya, S. K., Ahokas, R. A. & Gerling, I. C. Myofibroblast-mediated mechanisms of pathological remodelling of the heart. Nat. Rev. Cardiol. 10, 15–26 (2013).

    CAS  PubMed  Google Scholar 

  14. Weber, K. T. & Diez, J. Targeting the cardiac myofibroblast secretome to treat myocardial fibrosis in heart failure. Circ. Heart Fail. 9, e003315 (2016).

    PubMed  Google Scholar 

  15. Nag, A. C. Study of non-muscle cells of the adult mammalian heart: a fine structural analysis and distribution. Cytobios 28, 41–61 (1980).

    CAS  PubMed  Google Scholar 

  16. Banerjee, I., Fuseler, J. W., Price, R. L., Borg, T. K. & Baudino, T. A. Determination of cell types and numbers during cardiac development in the neonatal and adult rat and mouse. Am. J. Physiol. Heart Circ. Physiol. 293, H1883–H1891 (2007).

    CAS  PubMed  Google Scholar 

  17. Zak, R. Development and proliferative capacity of cardiac muscle cells. Circ. Res. 35 (Suppl. II), 17–26 (1974).

    CAS  Google Scholar 

  18. Pinto, A. R. et al. Revisiting cardiac cellular composition. Circ. Res. 118, 400–409 (2016).

    CAS  PubMed  Google Scholar 

  19. Caulfield, J. B. & Borg, T. K. The collagen network of the heart. Lab. Invest. 40, 364–372 (1979).

    CAS  PubMed  Google Scholar 

  20. Camelliti, P., Borg, T. K. & Kohl, P. Structural and functional characterisation of cardiac fibroblasts. Cardiovasc. Res. 65, 40–51 (2005).

    CAS  PubMed  Google Scholar 

  21. Smith, C. L., Baek, S. T., Sung, C. Y. & Tallquist, M. D. Epicardial-derived cell epithelial-to-mesenchymal transition and fate specification require PDGF receptor signaling. Circ. Res. 108, e15–e26 (2011).

    CAS  PubMed  PubMed Central  Google Scholar 

  22. Acharya, A. et al. The bHLH transcription factor Tcf21 is required for lineage-specific EMT of cardiac fibroblast progenitors. Development 139, 2139–2149 (2012).

    CAS  PubMed  PubMed Central  Google Scholar 

  23. Vaage, J. & Lindblad, W. J. Production of collagen type I by mouse peritoneal macrophages. J. Leukoc. Biol. 48, 274–280 (1990).

    CAS  PubMed  Google Scholar 

  24. Vaage, J. & Harlos, J. P. Collagen production by macrophages in tumour encapsulation and dormancy. Br. J. Cancer 63, 758–762 (1991).

    CAS  PubMed  PubMed Central  Google Scholar 

  25. Hayashi, M. et al. Secretion of collagen types I and II by epithelial and endothelial cells in the developing chick cornea demonstrated by in situ hybridization and immunohistochemistry. Development 103, 27–36 (1988).

    CAS  PubMed  Google Scholar 

  26. Alexakis, C., Partridge, T. & Bou-Gharios, G. Implication of the satellite cell in dystrophic muscle fibrosis: a self-perpetuating mechanism of collagen overproduction. Am. J. Physiol. Cell Physiol. 293, C661–C669 (2007).

    CAS  PubMed  Google Scholar 

  27. Liu, E. et al. Secreted collagen induced by ascorbic acid in L5 cloned muscle cultures does not affect acetylcholine receptor expression. Exp. Cell Res. 209, 76–81 (1993).

    CAS  PubMed  Google Scholar 

  28. Zanotti, S. et al. Altered extracellular matrix transcript expression and protein modulation in primary Duchenne muscular dystrophy myotubes. Matrix Biol. 26, 615–624 (2007).

    CAS  PubMed  Google Scholar 

  29. Borg, T. K., Johnson, L. D. & Lill, P. H. Specific attachment of collagen to cardiac myocytes: in vivo and in vitro. Dev. Biol. 97, 417–423 (1983).

    CAS  PubMed  Google Scholar 

  30. Fisher, S. A. & Periasamy, M. Collagen synthesis inhibitors disrupt embryonic cardiocyte myofibrillogenesis and alter the expression of cardiac specific genes in vitro. J. Mol. Cell. Cardiol. 26, 721–731 (1994).

    CAS  PubMed  Google Scholar 

  31. Kong, P., Christia, P., Saxena, A., Su, Y. & Frangogiannis, N. G. Lack of specificity of fibroblast-specific protein 1 in cardiac remodeling and fibrosis. Am. J. Physiol. Heart Circ. Physiol. 305, H1363–H1372 (2013).

    CAS  PubMed  PubMed Central  Google Scholar 

  32. Hudon-David, F., Bouzeghrane, F., Couture, P. & Thibault, G. Thy-1 expression by cardiac fibroblasts: lack of association with myofibroblast contractile markers. J. Mol. Cell. Cardiol. 42, 991–1000 (2007).

    CAS  PubMed  Google Scholar 

  33. Perez-Pomares, J. M., Macias, D., Garcia-Garrido, L. & Munoz-Chapuli, R. Contribution of the primitive epicardium to the subepicardial mesenchyme in hamster and chick embryos. Dev. Dyn. 210, 96–105 (1997).

    CAS  PubMed  Google Scholar 

  34. Zhang, S. et al. A host deficiency of discoidin domain receptor 2 (DDR2) inhibits both tumour angiogenesis and metastasis. J. Pathol. 232, 436–448 (2014).

    CAS  PubMed  Google Scholar 

  35. Goldsmith, E. C., Zhang, X., Watson, J., Hastings, J. & Potts, J. D. The collagen receptor DDR2 is expressed during early cardiac development. Anat. Rec. (Hoboken) 293, 762–769 (2010).

    CAS  Google Scholar 

  36. Zeisberg, E. M. & Kalluri, R. Origins of cardiac fibroblasts. Circ. Res. 107, 1304–1312 (2010).

    CAS  PubMed  PubMed Central  Google Scholar 

  37. Asli, N., Xaymardan, M. & Harvey, R. Epicardial origin of resident mesenchymal stem cells in the adult mammalian heart. J. Dev. Biol. 2, 117–137 (2014).

    CAS  Google Scholar 

  38. Gittenberger-de Groot, A. C., Vrancken Peeters, M. P., Mentink, M. M., Gourdie, R. G. & Poelmann, R. E. Epicardium-derived cells contribute a novel population to the myocardial wall and the atrioventricular cushions. Circ. Res. 82, 1043–1052 (1998).

    CAS  PubMed  Google Scholar 

  39. Mikawa, T. & Gourdie, R. G. Pericardial mesoderm generates a population of coronary smooth muscle cells migrating into the heart along with ingrowth of the epicardial organ. Dev. Biol. 174, 221–232 (1996).

    CAS  PubMed  Google Scholar 

  40. Dettman, R. W., Denetclaw, W. Jr, Ordahl, C. P. & Bristow, J. Common epicardial origin of coronary vascular smooth muscle, perivascular fibroblasts, and intermyocardial fibroblasts in the avian heart. Dev. Biol. 193, 169–181 (1998).

    CAS  PubMed  Google Scholar 

  41. Zhou, B. et al. Epicardial progenitors contribute to the cardiomyocyte lineage in the developing heart. Nature 454, 109–113 (2008).

    CAS  PubMed  PubMed Central  Google Scholar 

  42. Wessels, A. et al. Epicardially derived fibroblasts preferentially contribute to the parietal leaflets of the atrioventricular valves in the murine heart. Dev. Biol. 366, 111–124 (2012).

    CAS  PubMed  PubMed Central  Google Scholar 

  43. Cai, C. L. et al. A myocardial lineage derives from Tbx18 epicardial cells. Nature 454, 104–108 (2008).

    CAS  PubMed  PubMed Central  Google Scholar 

  44. Braitsch, C. M., Kanisicak, O., van Berlo, J. H., Molkentin, J. D. & Yutzey, K. E. Differential expression of embryonic epicardial progenitor markers and localization of cardiac fibrosis in adult ischemic injury and hypertensive heart disease. J. Mol. Cell. Cardiol. 65, 108–119 (2013).

    CAS  PubMed  Google Scholar 

  45. Zeisberg, E. M. et al. Endothelial-to-mesenchymal transition contributes to cardiac fibrosis. Nat. Med. 13, 952–961 (2007).

    CAS  PubMed  Google Scholar 

  46. Widyantoro, B. et al. Endothelial cell-derived endothelin-1 promotes cardiac fibrosis in diabetic hearts through stimulation of endothelial-to-mesenchymal transition. Circulation 121, 2407–2418 (2010).

    CAS  PubMed  Google Scholar 

  47. Haudek, S. B. et al. Bone marrow-derived fibroblast precursors mediate ischemic cardiomyopathy in mice. Proc. Natl Acad. Sci. USA 103, 18284–18289 (2006).

    CAS  PubMed  PubMed Central  Google Scholar 

  48. Mollmann, H. et al. Bone marrow-derived cells contribute to infarct remodelling. Cardiovasc. Res. 71, 661–671 (2006).

    PubMed  Google Scholar 

  49. van Amerongen, M. J. et al. Bone marrow-derived myofibroblasts contribute functionally to scar formation after myocardial infarction. J. Pathol. 214, 377–386 (2008).

    CAS  PubMed  Google Scholar 

  50. Ieronimakis, N. et al. Coronary adventitial cells are linked to perivascular cardiac fibrosis via TGFbeta1 signaling in the mdx mouse model of Duchenne muscular dystrophy. J. Mol. Cell. Cardiol. 63, 122–134 (2013).

    CAS  PubMed  Google Scholar 

  51. Kramann, R. et al. Perivascular Gli1+ progenitors are key contributors to injury-induced organ fibrosis. Cell Stem Cell 16, 51–66 (2015).

    CAS  PubMed  Google Scholar 

  52. van Wijk, B., Gunst, Q. D., Moorman, A. F. & van den Hoff, M. J. Cardiac regeneration from activated epicardium. PLoS ONE 7, e44692 (2012).

    CAS  PubMed  PubMed Central  Google Scholar 

  53. Zhou, B. et al. Adult mouse epicardium modulates myocardial injury by secreting paracrine factors. J. Clin. Invest. 121, 1894–1904 (2011).

    CAS  PubMed  PubMed Central  Google Scholar 

  54. Clausen, B. E., Burkhardt, C., Reith, W., Renkawitz, R. & Forster, I. Conditional gene targeting in macrophages and granulocytes using LysMcre mice. Transgenic Res. 8, 265–277 (1999).

    CAS  PubMed  Google Scholar 

  55. van Berlo, J. H. et al. c-Kit+ cells minimally contribute cardiomyocytes to the heart. Nature 509, 337–341 (2014).

    CAS  PubMed  PubMed Central  Google Scholar 

  56. Ubil, E. et al. Mesenchymal-endothelial transition contributes to cardiac neovascularization. Nature 514, 585–590 (2014).

    CAS  PubMed  PubMed Central  Google Scholar 

  57. Ruiz-Villalba, A. et al. Interacting resident epicardium-derived fibroblasts and recruited bone marrow cells form myocardial infarction scar. J. Am. Coll. Cardiol. 65, 2057–2066 (2015).

    PubMed  Google Scholar 

  58. Ivanova, A. et al. In vivo genetic ablation by Cre-mediated expression of diphtheria toxin fragment A. Genesis 43, 129–135 (2005).

    CAS  PubMed  PubMed Central  Google Scholar 

  59. Snider, P. et al. Origin of cardiac fibroblasts and the role of periostin. Circ. Res. 105, 934–947 (2009).

    CAS  PubMed  PubMed Central  Google Scholar 

  60. Snider, P. et al. Periostin is required for maturation and extracellular matrix stabilization of noncardiomyocyte lineages of the heart. Circ. Res. 102, 752–760 (2008).

    CAS  PubMed  PubMed Central  Google Scholar 

  61. Qian, L. et al. In vivo reprogramming of murine cardiac fibroblasts into induced cardiomyocytes. Nature 485, 593–598 (2012).

    CAS  PubMed  PubMed Central  Google Scholar 

  62. Duim, S. N., Kurakula, K., Goumans, M. J. & Kruithof, B. P. Cardiac endothelial cells express Wilms' tumor-1: Wt1 expression in the developing, adult and infarcted heart. J. Mol. Cell. Cardiol. 81, 127–135 (2015).

    CAS  PubMed  Google Scholar 

  63. Guimaraes-Camboa, N. et al. Pericytes of multiple organs do not behave as mesenchymal stem cells in vivo. Cell Stem Cell 20, 345–359.e5 (2017).

    CAS  PubMed  PubMed Central  Google Scholar 

  64. Fujiu, K. & Nagai, R. Fibroblast-mediated pathways in cardiac hypertrophy. J. Mol. Cell. Cardiol. 70, 64–73 (2014).

    CAS  PubMed  Google Scholar 

  65. Willems, I. E., Havenith, M. G., De Mey, J. G. & Daemen, M. J. The alpha-smooth muscle actin-positive cells in healing human myocardial scars. Am. J. Pathol. 145, 868–875 (1994).

    CAS  PubMed  PubMed Central  Google Scholar 

  66. Bergmann, O. et al. Dynamics of cell generation and turnover in the human heart. Cell 161, 1566–1575 (2015).

    CAS  PubMed  Google Scholar 

  67. Mewton, N., Liu, C. Y., Croisille, P., Bluemke, D. & Lima, J. A. Assessment of myocardial fibrosis with cardiovascular magnetic resonance. J. Am. Coll. Cardiol. 57, 891–903 (2011).

    PubMed  Google Scholar 

  68. Tziakas, D. N. et al. Independent and additive prognostic ability of serum carboxy-terminal telopeptide of collagen type-I in heart failure patients: a multi-marker approach with high-negative predictive value to rule out long-term adverse events. Eur. J. Prev. Cardiol. 19, 62–71 (2012).

    PubMed  Google Scholar 

  69. Ellims, A. H. et al. Evaluating the utility of circulating biomarkers of collagen synthesis in hypertrophic cardiomyopathy. Circ. Heart Fail. 7, 271–278 (2014).

    CAS  PubMed  Google Scholar 

  70. Kupari, M., Laine, M., Turto, H., Lommi, J. & Werkkala, K. Circulating collagen metabolites, myocardial fibrosis and heart failure in aortic valve stenosis. J. Heart Valve Dis. 22, 166–176 (2013).

    PubMed  Google Scholar 

  71. Gyongyosi, M. et al. Myocardial fibrosis: biomedical research from bench to bedside. Eur. J. Heart Fail. 19, 177–191 (2017).

    PubMed  Google Scholar 

  72. Ravassa, S. et al. Phenotyping of myocardial fibrosis in hypertensive patients with heart failure. Influence on clinical outcome. J. Hypertens. 35, 853–861 (2017).

    CAS  PubMed  Google Scholar 

  73. Ho, J. E. et al. Galectin-3, a marker of cardiac fibrosis, predicts incident heart failure in the community. J. Am. Coll. Cardiol. 60, 1249–1256 (2012).

    CAS  PubMed  PubMed Central  Google Scholar 

  74. Lopez-Andres, N. et al. Association of galectin-3 and fibrosis markers with long-term cardiovascular outcomes in patients with heart failure, left ventricular dysfunction, and dyssynchrony: insights from the CARE-HF (Cardiac Resynchronization in Heart Failure) trial. Eur. J. Heart Fail. 14, 74–81 (2012).

    CAS  PubMed  Google Scholar 

  75. Villar, A. V. et al. Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patients. Int. J. Cardiol. 167, 2875–2881 (2013).

    PubMed  Google Scholar 

  76. Beaumont, J. et al. MicroRNA-19b is a potential biomarker of increased myocardial collagen cross-linking in patients with aortic stenosis and heart failure. Sci. Rep. 7, 40696 (2017).

    CAS  PubMed  PubMed Central  Google Scholar 

  77. Bunt, S. et al. Hemocyte-secreted type IV collagen enhances BMP signaling to guide renal tubule morphogenesis in Drosophila. Dev. Cell 19, 296–306 (2010).

    CAS  PubMed  PubMed Central  Google Scholar 

  78. Bunt, S., Denholm, B. & Skaer, H. Characterisation of the Drosophila procollagen lysyl hydroxylase, dPlod. Gene Expr. Patterns 11, 72–78 (2011).

    CAS  PubMed  PubMed Central  Google Scholar 

  79. Shahab, J. et al. Loss of SPARC dysregulates basal lamina assembly to disrupt larval fat body homeostasis in Drosophila melanogaster. Dev. Dyn. 244, 540–552 (2015).

    CAS  PubMed  Google Scholar 

  80. Zang, Y. et al. Plasma membrane overgrowth causes fibrotic collagen accumulation and immune activation in Drosophila adipocytes. eLife 4, e07187 (2015).

    PubMed  PubMed Central  Google Scholar 

  81. Pastor-Pareja, J. C. & Xu, T. Shaping cells and organs in Drosophila by opposing roles of fat body-secreted collagen IV and perlecan. Dev. Cell 21, 245–256 (2011).

    CAS  PubMed  PubMed Central  Google Scholar 

  82. Stempien-Otero, A., Kim, D. H. & Davis, J. Molecular networks underlying myofibroblast fate and fibrosis. J. Mol. Cell. Cardiol. 97, 153–161 (2016).

    CAS  PubMed  PubMed Central  Google Scholar 

  83. Derynck, R. & Zhang, Y. E. Smad-dependent and Smad-independent pathways in TGF-beta family signalling. Nature 425, 577–584 (2003).

    CAS  PubMed  Google Scholar 

  84. Stambe, C. et al. The role of p38alpha mitogen-activated protein kinase activation in renal fibrosis. J. Am. Soc. Nephrol. 15, 370–379 (2004).

    CAS  PubMed  Google Scholar 

  85. Wang, L., Ma, R., Flavell, R. A. & Choi, M. E. Requirement of mitogen-activated protein kinase kinase 3 (MKK3) for activation of p38alpha and p38delta MAPK isoforms by TGF-beta 1 in murine mesangial cells. J. Biol. Chem. 277, 47257–47262 (2002).

    CAS  PubMed  Google Scholar 

  86. Davis, J., Burr, A. R., Davis, G. F., Birnbaumer, L. & Molkentin, J. D. A. TRPC6-dependent pathway for myofibroblast transdifferentiation and wound healing in vivo. Dev. Cell 23, 705–715 (2012).

    CAS  PubMed  PubMed Central  Google Scholar 

  87. Furtado, M. B. et al. Cardiogenic genes expressed in cardiac fibroblasts contribute to heart development and repair. Circ. Res. 114, 1422–1434 (2014).

    CAS  PubMed  PubMed Central  Google Scholar 

  88. Kaur, H. et al. Targeted ablation of periostin-expressing activated fibroblasts prevents adverse cardiac remodeling in mice. Circ. Res. 118, 1906–1917 (2016).

    CAS  PubMed  Google Scholar 

  89. van Putten, S., Shafieyan, Y. & Hinz, B. Mechanical control of cardiac myofibroblasts. J. Mol. Cell. Cardiol. 93, 133–142 (2016).

    CAS  PubMed  Google Scholar 

  90. Gabbiani, G., Hirschel, B. J., Ryan, G. B., Statkov, P. R. & Majno, G. Granulation tissue as a contractile organ. A study of structure and function. J. Exp. Med. 135, 719–734 (1972).

    CAS  PubMed  PubMed Central  Google Scholar 

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Acknowledgements

We thank Jill T. Kuwabara from the Tallquist Laboratory, University of Hawaii, USA, for the original images in Figure 3.

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Both authors researched data for the article, discussed its content, wrote the manuscript, and reviewed/edited it before submission.

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Correspondence to Michelle D. Tallquist or Jeffery D. Molkentin.

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Tallquist, M., Molkentin, J. Redefining the identity of cardiac fibroblasts. Nat Rev Cardiol 14, 484–491 (2017). https://doi.org/10.1038/nrcardio.2017.57

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