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Updated: Jun 24, 2026

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Published on: September 8, 2017
Endothelium-driven myocardial growth or nitric oxide at the crossroads
Daniela Tirziu1, Michael Simons
1Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.
Insights
The heart
Area of Science:
- Cardiovascular Biology
- Cardiac Physiology
- Endothelial Function
Background:
- The endothelium in the heart and coronary vasculature acts as a sensor.
- It facilitates communication between endothelial cells and cardiac myocytes.
- Endothelium-derived factors, like nitric oxide, influence cardiac cells.
Purpose of the Study:
- To review recent findings on endothelium-to-myocyte signaling.
- To highlight the role of nitric oxide in regulating cardiac hypertrophy.
- To focus on paracrine signaling mechanisms.
Main Methods:
- Literature review of recent data.
- Analysis of signaling pathways.
- Focus on nitric oxide's paracrine effects.
Main Results:
- Nitric oxide signaling from endothelium affects cardiac myocytes.
- This signaling pathway plays a role in myocardial hypertrophy.
- Endothelium-to-myocyte communication is crucial for cardiac regulation.
Conclusions:
- Endothelium-derived nitric oxide is a key regulator of cardiac hypertrophy.
- Paracrine signaling via nitric oxide mediates important cardiac functions.
- Understanding this pathway is vital for cardiac health.
Abstract:
Endothelium lining the coronary vasculature and the heart chambers is a dynamic sensor that serves a variety of functions including bidirectional communications with cardiac myocytes. Among endothelium-released factors, nitric oxide exerts multifactorial effects on various cell types in the heart and may play a role in growth of the vasculature and myocardial hypertrophy. This review summarizes new data regarding the endothelium-to-myocyte signaling focusing on its role in regulation of cardiac hypertrophy through a nitric-oxide-mediated paracrine signal.
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