Here, we describe the successes and challenges in cardiac AAV gene therapy, a treatment modality that has the potential to transform current treatment approaches for cardiac diseases.
Our data indicate that subjects with the ABCA1R219K variant may get significantly less heart disease risk reduction from pravastatin treatment than those without the variant.
An observational single center study was conducted to examine 4901 consecutive patients with heart disease receiving coronary angiography and ABO group determination at National Research Council Institute of Clinical Physiology between January 1993 and December 2003, with maximum 10 years follow-up.
On the contrary, established proteomic technologies, together with the new alternative strategies currently under evaluation (i.e. metabolomics), are now making possible the translation of data obtained on the bench to the daily clinical routine with the discovery of new diagnostic/prognostic biomarkers (such as troponin for ACS and BNP for congestive heart failure) and the identification of new therapeutic approaches for combating heart diseases.
The Angiotensin Converting Enzyme (ACE) gene may influence the risk of heart disease and the response to various forms of exercise training may be at least partly dependent on the ACE genotype.
Recent meta-analysis of large clinical trials on the use of ACE inhibitors and angiotensin receptor blockers in cardiovascular disease has demonstrated an imbalance between patients that significantly benefit from these therapeutic agents and those that remain at risk for heart disease progression.
The previously described relationship between heart disease and the ACE-gene polymorphism in diabetes could thus be founded in an increased extent of atherosclerosis among patients with the ID- and DD-ACE-gene subtypes.
Our results showed that the D allele of ACE was significantly associated with an increased risk of HDs in the Asian and European groups but not in the American group.
The ThrThr genotype of the angiotensinogen (AGT) Met235Thr polymorphism has been associated with elevated AGT levels, hypertension, increased heart disease risk, and improved blood pressure (BP) response to angiotensin-converting enzyme (ACE) inhibitors.
Angiotensin converting enzyme (ACE) polymorphism has been shown to be important in hypertension progression and also in diabetes complications, especially associated with heart disease.
Thirty-one dogs (20 wild-type, 11 ACE polymorphism) with heart disease were evaluated with ACE activity measurement and systolic blood pressure before and after administration of an ACE inhibitor (enalapril).
In this study of 104 Chinese patients with end-stage heart failure due to idiopathic dilated or ischemic cardiomyopathy, the DD genotype frequency was low (12% and 11%, respectively) and was not seen more often than in a control group of 183 subjects without cardiac disease (13%).
In conclusion, our findings confirmed cardioprotective effects of SIRT6 on pathological remodeling, fibrosis and myocardial injury through activation of AMPK-ACE2 signaling and suppression of CTGF-FKN pathway, indicating that SIRT6 functions as a partial agonist of ACE2 and targeting SIRT6 has potential therapeutic importance for cardiac fibrosis and heart disease.
In conclusion, ACE2 plays a novel role in heart disease associated with obesity wherein ACE2 negatively regulates obesity-induced EAT inflammation and cardiac insulin resistance.