Cardiac fibrosis in the ageing heart: Contributors and mechanisms

Lu Lu, Jingbin Guo, Yue Hua, Kevin Huang, Ruth Magaye, Jake Cornell, Darren J. Kelly, Christopher Reid, Danny Liew, Yingchun Zhou, Aihua Chen, Wei Xiao, Qiang Fu, Bing Hui Wang

Research output: Contribution to journalArticleResearchpeer-review

34 Citations (Scopus)


Cardiac fibrosis refers to an excessive deposition of extracellular matrix (ECM) in cardiac tissue. Fibrotic tissue is stiffer and less compliant, resulting in subsequent cardiac dysfunction and heart failure. Cardiac fibrosis in the ageing heart may involve activation of fibrogenic signalling and inhibition of anti-fibrotic signalling, leading to an imbalance of ECM turnover. Excessive accumulation of ECM such as collagen in older patients contributes to progressive ventricular dysfunction. Overexpression of collagen is derived from various sources, including higher levels of fibrogenic growth factors, proliferation of fibroblasts and cellular transdifferentiation. These may be triggered by factors, such as oxidative stress, inflammation, hypertension, cellular senescence and cell death, contributing to age-related fibrotic cardiac remodelling. In this review, we will discuss the fibrogenic contributors in age-related cardiac fibrosis, and the potential mechanisms by which fibrogenic processes can be interrupted for therapeutic intent.

Original languageEnglish
Pages (from-to)55-63
Number of pages9
JournalClinical and Experimental Pharmacology and Physiology
Issue numberS1
Publication statusPublished - 1 Dec 2017


  • ageing
  • cardiac fibrosis
  • extracellular matrix turnover
  • fibrogenic factors
  • heart failure

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