Investigational drugs targeting cardiac fibrosis

Abstract

Fibrosis is an accumulation of proteins including collagen in the extracellular space, which has previously been considered as irreversible damage in various cardiovascular diseases including heart failure and hypertension. The pathophysiology of fibrosis is currently better understood and can be evaluated by non-invasive methods. Here, the authors present briefly the impact and molecular mechanisms of fibrosis in the myocardium and the promising therapeutic candidates including anti-hypertensive therapies, heart-rate lowering drugs, anti-inflammatory agents, as well as other innovative approaches such as inhibitors of growth factors, miRNA or cell therapy. Surrogate end points allow for larger clinical trials than previously possible with endomyocardial biopsies, and magnetic resonance and molecular imaging should open new fields of research on cardiac fibrosis. Several pre-clinical findings are very promising, and some clinical data support the proofs of concept, mainly those with inhibitors of the renin-angiotensin system. These approaches open the field for regression of fibrosis and include the following: first, some of these drugs are widely used like renin-angiotensin system inhibitors; second, inflammation modulators; third, in near future entirely new approaches targeting the TGF-β pathways, or others like cell therapies or genetic interventions.

Functions of Galectin-3 and Its Role in Fibrotic Diseases

“…Cardiac fibrosis is considered irreversible damage in various cardiovascular diseases, among them overt heart failure (HF) (Roubille et al, 2014). However, the diagnosis and potential treatments of cardiac fibrosis are limited.…”

Is galectin-3 a promoter of ventricular dysfunction?

“…Myocardial fibrosis is considered irreversible in a wide range of cardiovascular diseases, including overt HF [41]. Recent studies have shown that galectin-3 is involved in the proliferation and differentiation of myofibroblasts that further stimulate collagen synthesis.…”

Ventricular Remodeling after Myocardial Infarct: A Minireview on the Impact of Obstructive Sleep Apnea Syndrome

“…Other targets, such as tissue fibrosis, may be left untreated [8] . Whether the presence of OSAS could impact the post-MI remodeling is unclear.…”