Healing Hearts: How Angiotensin 1-7 Could Revolutionize Cardiac Recovery After Heart Attacks
"Discover how the naturally occurring peptide Angiotensin 1-7 (Ang(1-7)) could promote cardiac repair and improve heart function post-infarction."
When a heart attack, or myocardial infarction (MI), strikes, the heart's battle to repair itself begins. This repair involves angiogenesis, the growth of new blood vessels, and inflammatory responses in the damaged heart tissue. This process helps maintain the heart's structural integrity and is vital for recovery. However, sometimes, the heart can remodel in ways that aren't helpful, leading to fibrosis (stiffening of tissue) and hypertrophy (enlargement) in the undamaged areas.
Scientists have been focusing on what controls this repair and remodeling. The renin-angiotensin system (RAS), a hormone system that regulates blood pressure and fluid balance, plays a significant role. Angiotensin II (AngII), a key player in the RAS, can stimulate processes that lead to repair but also remodeling. Recently, a new understanding of the RAS has emerged with the discovery of angiotensin-converting enzyme 2 (ACE2).
ACE2 generates Angiotensin (1-7) [Ang(1-7)], which interacts with Mas receptors to trigger protective cellular actions. Ang(1-7) has shown promise in countering issues such as apoptosis (cell death), fibrosis, and hypertrophy in the heart following an MI. In this article, we delve into how Ang(1-7) might regulate angiogenesis and improve heart function after a heart attack.
Ang(1-7): A Key to Cardiac Angiogenesis?
The study investigates whether Ang(1-7) regulates cardiac angiogenesis and contributes to cardiac repair. The research involved examining the expression of ACE2 and Mas receptors in rats post-MI, alongside administering a Mas receptor antagonist (A779) to assess Ang(1-7)'s role.
- Creating an MI Model: Left ventricular anterior transmural MI was induced in female Sprague Dawley rats through permanent ligation of the left coronary artery.
- Monitoring ACE2 and Mas Receptor Expression: The levels of ACE2 and Mas receptors in the heart tissue were tracked over time in both control and MI rats.
- Administering A779: Some MI rats were treated with A779, a Mas receptor antagonist, to block the effects of Ang(1-7).
- Assessing Vascular Density: The growth of new blood vessels in the infarcted area was quantified using CD31 staining, a marker for vascular endothelial cells.
- Evaluating Cardiac Function: Echocardiography was performed to assess heart function, including left ventricular dimensions and fraction shortening.
- Measuring Angiogenic Mediators: The expression of various factors involved in angiogenesis, such as VEGF-D and MMP-9, was measured using RT-PCR.
What the Study Tells Us
The study reveals that Ang(1-7) promotes angiogenesis in the infarcted myocardium by stimulating the expression of VEGF-D and MMP-9. Blocking Mas receptors with A779 reduced vascular density and impaired ventricular function, highlighting the importance of Ang(1-7) signaling in cardiac repair. This suggests that Ang(1-7) could be a therapeutic target for improving cardiac function post-MI. More research is needed to fully understand the potential of Ang(1-7) in cardiac care.