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Published on: June 14, 2016
In vitro inhibitory effects of atorvastatin on cardiac fibroblasts: implications for ventricular remodelling
Jennifer Martin1, Rachel Denver, Michael Bailey
1National Health and Medical Research Council of Australia Centre for Clincial Research and Excellence in Therapeutics, Epidemiology and Preventive Medicine, Monash University/Alfred Hospital, Melbourne, Victoria, Australia. jhmartin@medstv.unimelb.edu.au
Insights
Statins like atorvastatin inhibit collagen production in cardiac fibroblasts, potentially reducing adverse remodeling after myocardial infarction. This antifibrotic effect may contribute to their cardiovascular benefits.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Cell Biology
Background:
- Statins (HMG CoA reductase inhibitors) reduce mortality post-myocardial infarction (MI).
- Beyond anti-ischaemic effects, statins may offer other benefits.
- Pathological extracellular matrix deposition is key in post-MI remodeling.
Purpose of the Study:
- To investigate if atorvastatin inhibits extracellular matrix production in cardiac fibroblasts in vitro.
- To explore the antifibrotic potential of atorvastatin.
Main Methods:
- Primary rat and human cardiac fibroblasts were cultured.
- Cells were stimulated with transforming growth factor-beta1 (TGF-beta1) or angiotensin II (Ang II).
- Atorvastatin's effect on collagen synthesis, procollagen mRNA, and connective tissue growth factor gene expression was measured.
Main Results:
- Atorvastatin significantly reduced collagen synthesis in a dose-dependent manner when cells were stimulated with TGF-beta1 or Ang II.
- Similar antifibrotic effects were observed in human cardiac fibroblasts.
- Atorvastatin decreased TGF-beta1 and Ang II-induced increases in alpha(I)-procollagen mRNA and connective tissue growth factor expression.
Conclusions:
- Atorvastatin directly inhibits collagen production by cardiac fibroblasts.
- This antifibrotic action of atorvastatin may contribute to its beneficial effects on cardiac remodeling after MI.
Abstract:
1. Hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (statins) reduce mortality after myocardial infarction (MI). Although this may be predominantly due to their known anti-ischaemic actions, these drugs are known to have other beneficial effects. 2. Because pathological deposition of extracellular matrix (ECM) material is a key component of remodelling after MI, we sought to determine whether atorvastatin could inhibit ECM production in vitro. 3. The addition of atorvastatin to rat cardiac fibroblasts stimulated with either transforming growth factor (TGF)-beta1 (TGF-beta1) or angiotensin (Ang) II reduced collagen synthesis in a dose-dependent manner (3.7-fold reduction (95% confidence interval (CI) 1.8-15; P < 0.01) and 5.3-fold reduction (95% CI 1.8-7.7; P < 0.01), respectively, compared with stimulant alone). Similar observations were made in human cardiac fibroblast cell culture. Atorvastatin also dose-dependently reduced TGF-beta1 and AngII-induced increases in alpha(I)-procollagen mRNA (P < 0.01 for both), as well as gene expression of the profibrotic peptide connective tissue growth factor. 4. Atorvastatin appears to directly inhibit collagen production by cardiac fibroblasts. This antifibrotic action may contribute to the antiremodelling effect of statins.
