Some studies have suggested that microRNA-133a could reduce cardiac hypertrophy and myocardial fibrosis.

The mechanism by which SGLT2 inhibitors reduce cardiac events in diabetic patients remains unclear.

Dual antiplatelet therapy with aspirin and a thienopyridine has been shown to reduce cardiac events after coronary stenting.

These orally active EET agonists lower blood pressure and reduce cardiac and renal injury in spontaneous and angiotensin hypertension.

In conclusion, these findings suggest that EET analog EET-B has beneficial therapeutic actions to reduce cardiac remodeling in SHR subjected to MI.

Conclusions: Lifestyle intervention significantly attenuates the development of an HRE but does not reduce cardiac size after 1 yr in patients with type 2 diabetes.

Conversely, late activation of beta-catenin signaling reduces cardiac differentiation in ES cells.

It also reduced cardiac hypertrophy and proteinuria developed in GB hypertensive rats.

All four compounds significantly reduced cardiac work and its first derivative.

Results: GT reduced cardiac hypertrophy and improved systolic and diastolic dysfunction.

TUDCA administration also reduced cardiac apoptosis and the related proteins in the TUDCA-TAC group.

Such TH-related signaling events are associated with reduced cardiac inflammation, apoptosis, and mitochondrial injury.

Recent studies implicate increased cGMP synthesis as a postreceptor contributor to reduced cardiac sympathetic responsiveness.

Its beneficial effects may, however, be associated with reduced cardiac fibrosis, oxidative stress and expression of pro-inflammatory cytokines.

Verapamil in particular, moderated emotional arousal, the vasoconstrictive response and reduced cardiac load without lowering cardiac output demands.

Carvedilol reduced cardiac expression of interleukin-1beta but did not prevent cardiac fetal gene re-expression or modify cardiac oxidative stress.