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Review
. 2015 Mar 17;131(11):1019-30.
doi: 10.1161/CIRCULATIONAHA.114.008788.

Immune cell and other noncardiomyocyte regulation of cardiac hypertrophy and remodeling

Ryan A Frieler  1 , Richard M Mortensen  2
Affiliations
Review

Immune cell and other noncardiomyocyte regulation of cardiac hypertrophy and remodeling

Ryan A Frieler et al. Circulation. .
No abstract available

Keywords: fibrosis; heart failure; hypertrophy; immune system; ventricular remodeling.

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Conflict of interest statement

Conflict of Interest Disclosures: None.

Figures

Figure 1
Figure 1
Overview of cardiomyocyte and non-cardiomyocyte interactions during cardiac hypertrophy and remodeling. Cardiomyocytes respond to pathogenic stimuli by secreting inflammatory cytokines, chemokines, and DAMPs, which are recognized by local non-cardiomyocyte cells. This induces activation and expansion of resident macrophages and fibroblasts, and also recruits bone marrow-derived immune cells from the circulation. Activated immune cells and fibroblasts secrete both pro-hypertrophic and pro-fibrotic cytokines, which induce cardiomyocyte hypertrophy and promote fibroblast differentiation, matrix deposition, and interstitial fibrosis.
Figure 2
Figure 2
Detailed hypertrophic and fibrotic signaling mechanisms between cardiac cells. Interactions between cardiac cells involve complex signaling pathways that induce phenotypic changes in nearby cells. Hypertrophy and fibrosis can be augmented by pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and pro-fibrotic and molecules (TGF-β, angiotensin-II). RAAS activation has direct pro-inflammatory, pro-hypertrophic, and pro-fibrotic effects in cardiac cells, and these responses are pharmacologically inhibited with ACE inhibitors, ARBs, and MR antagonists. Tregs and exogenous IL-10 treatment can also suppress inflammation and hypertrophic signaling.
See this image and copyright information in PMC

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