期刊
JOURNAL OF CLINICAL MEDICINE
卷 6, 期 5, 页码 -出版社
MDPI
DOI: 10.3390/jcm6050053
关键词
fibrosis; cardiac fibroblast; myofibroblast; mechanotransduction; stiffness; extracellular matrix; integrins; syndecan; cytoskeleton; linker of the nucleoskeleton and cytoskeleton
资金
- Research Council of Norway, Anders Jahre's Fund for the Promotion of Science
- South-Eastern Regional Health Authority, Norway
- Simon Fougner Hartmanns Family Fund, Denmark
- European Commission Marie Curie Actions' COFUND program
- California Institute of Regenerative Medicine [RT3-07899]
- National Biomedical Computation Resource (NIH) [P41 GM103426]
- NIH R01 [HL105242, HL121754, HL137100]
- NIH U01 [HL121754, HL126273]
Cardiac fibrosis, the excessive accumulation of extracellular matrix (ECM), remains an unresolved problem in most forms of heart disease. In order to be successful in preventing, attenuating or reversing cardiac fibrosis, it is essential to understand the processes leading to ECM production and accumulation. Cardiac fibroblasts are the main producers of cardiac ECM, and harbor great phenotypic plasticity. They are activated by the disease-associated changes in mechanical properties of the heart, including stretch and increased tissue stiffness. Despite much remaining unknown, an interesting body of evidence exists on how mechanical forces are translated into transcriptional responses important for determination of fibroblast phenotype and production of ECM constituents. Such mechanotransduction can occur at multiple cellular locations including the plasma membrane, cytoskeleton and nucleus. Moreover, the ECM functions as a reservoir of pro-fibrotic signaling molecules that can be released upon mechanical stress. We here review the current status of knowledge of mechanotransduction signaling pathways in cardiac fibroblasts that culminate in pro-fibrotic gene expression.
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