Journal
CARDIOVASCULAR RESEARCH
Volume 102, Issue 2, Pages 290-301Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvu039
Keywords
Paracrine communication; Cardiomyocyte; Cardiac fibroblast; MicroRNAs; Cardiac remodelling; Therapeutics
Categories
Funding
- Integrated Research and Treatment Center [BMBF 01EO0802]
- Deutsche Forschungsgemeinschaft [DFG TH903/10-1]
- 7th European Framework programme (FIBROTARGET)
- internal Hannover Biomedical Research School (HBRS) programms Regenerative Sciences and Molecular Medicine
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Cardiac hypertrophy and fibrosis are two closely related adaptive response mechanisms of the myocardium to mechanical, metabolic, and genetic stress that finally contribute to the development of heart failure (HF). This relation is based on a dynamic interplay between many cell types including cardiomyocytes and fibroblasts during disease progression. Both cell types secrete a variety of growth factors, cytokines, and hormones that influence hypertrophic cardiomyocyte growth and fibrotic fibroblast activation in a paracrine and autocrine manner. It has become evident that, aside proteinous signals, microRNAs (miRNAs) and possible other RNA species such as long non-coding RNAs are potential players in such a cell-to-cell communication. By directly acting as paracrine signals or by modulating downstream intercellular signalling mediators, miRNAs can act as moderators of the intercellular crosstalk. These small regulators can potentially be secreted in a mircrine fashion, so that miRNAs can be assumed as the message itself. This review will summarize the recent findings about the paracrine crosstalk between cardiac fibroblasts and cardiomyocytes and addresses how miRNAs may be involved in this interplay. It also highlights therapeutic strategies targeting factors of pathological communication for the treatment of HF.
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