Skip to main content
Figure 3 | Molecular Medicine

Figure 3

From: Targeting Inflammation in Heart Failure with Histone Deacetylase Inhibitors

Figure 3

HDAC inhibitors target multiple cell types and mechanisms controlling heart failure. Stresses such as hypertension and MI can trigger remodeling of the heart, resulting in impaired systolic and diastolic function and, ultimately, heart failure. Inflammation contributes to cardiac remodeling, in part, by stimulating fibroblasts to produce excess extracellular matrix (ECM). HDAC inhibitors appear to block several pathogenic mechanisms controlling heart failure, including inflammation, EndoMT and fibroblast signaling, as well as myocyte hypertrophy and death. The antiinflammatory effects of HDAC inhibitors could be governed by induction of Tregs, although this hypothesis has not been tested in heart failure models. Thus, HDAC inhibitors intervene with heart failure progression at multiple steps that are downstream of the cell surface receptors targeted by standards-of-care, such as β-blockers, ACEi and ARBs. The unique mechanisms-of-action of HDAC inhibitors provide intriguing possibilities for disease modulation and synergy with current standards-of-care for heart failure.

Back to article page