Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 Aug;1(5):247-258.

Responses of Endothelial Cells Towards Ischemic Conditioning Following Acute Myocardial Infarction

Sauri Hernández-Reséndiz  1   2   3 , Mónica Muñoz-Vega  4 , Whendy E Contreras  1   2 , Gustavo E Crespo-Avilan  1   2 , Julian Rodriguez-Montesinos  5 , Oscar Arias-Carrión  6 , Oscar Pérez-Méndez  6 , William A Boisvert  7   8 , Klaus T Preissner  7   5 , Hector A Cabrera-Fuentes  1   2   3   7   5
Affiliations

Responses of Endothelial Cells Towards Ischemic Conditioning Following Acute Myocardial Infarction

Sauri Hernández-Reséndiz et al. Cond Med. 2018 Aug.

Abstract

One of the primary therapeutic goals of modern cardiology is to design strategies aimed at minimizing myocardial infarct size and optimizing cardiac function following acute myocardial infarction (AMI). Patients with AMI who underwent reperfusion therapy display dysfunction of the coronary endothelium. Consequently, ischemic endothelial cells become more permeable and weaken their natural anti-thrombotic and anti-inflammatory potential. Ischemia-reperfusion injury (IRI) is associated with activation of the humoral and cellular components of the hemostatic and innate immune system, and also with excessive production of reactive oxygen species (ROS), the inhibition of nitric oxide synthase, and with inflammatory processes. Given its essential role in the regulation of vascular homeostasis, involving platelets and leukocytes among others, dysfunctional endothelium can lead to increased risk of coronary vasospasm and thrombosis. Endothelial dysfunction can be prevented by ischemic conditioning with a protective intervention based on limited intermittent periods of ischemia and reperfusion. The molecular mechanisms and signal transduction pathways underlying conditioning phenomena in the coronary endothelium have been described as involving less ROS production, reduced adhesion of neutrophils to endothelial cells and diminished inflammatory reactions. This review summarizes our current understanding of the cellular and molecular mechanisms regulating IRI-affected and -damaged coronary endothelium, and how ischemic conditioning may preserve its function.

Keywords: cardioprotection; endothelium; inflammation; ischemia reperfusion injury; ischemic conditioning.

PubMed Disclaimer

Conflict of interest statement

Conflicts of interest The authors declare that they have no conflicts of interest.

Figures

Figure 1:
Figure 1:. Overview of endothelial cell responses towards acute myocardial infarction.
This scheme depicts the reperfusion-induced damage of endothelial cells following acute myocardial infarction.
Figure 2.
Figure 2.. Cardio-protective mediators and molecular mechanisms that are activated by ischemic conditioning in endothelial cells.
The illustration enumerates three necessary steps to explain cellular responses after ischemic conditioning induced cardioprotection.
See this image and copyright information in PMC

References

    1. Ampofo E, Lachnitt N, Rudzitis-Auth J, Schmitt BM, Menger MD, Laschke MW (2017) Indole-3-carbinol is a potent inhibitor of ischemia-reperfusion-induced inflammation. J Surg Res 215:34–46. - PubMed
    1. Anderson TJ, Uehata A, Gerhard MD, Meredith IT, Knab S, Delagrange D, Lieberman EH, Ganz P, Creager MA, Yeung AC, et al. (1995) Close relation of endothelial function in the human coronary and peripheral circulations. Journal of the American College of Cardiology 26:1235–1241. - PubMed
    1. Aoki M, Nata T, Morishita R, Matsushita H, Nakagami H, Yamamoto K, Yamazaki K, Nakabayashi M, Ogihara T, Kaneda Y (2001) Endothelial apoptosis induced by oxidative stress through activation of NF-kappaB: antiapoptotic effect of antioxidant agents on endothelial cells. Hypertension 38:48–55. - PubMed
    1. Asai M, Takeuchi K, Saotome M, Urushida T, Katoh H, Satoh H, Hayashi H, Watanabe H (2009) Extracellular acidosis suppresses endothelial function by inhibiting store-operated Ca2+ entry via non-selective cation channels. Cardiovasc Res 83:97–105. - PubMed
    1. Auchampach JA, Gross GJ (1993) Adenosine A1 receptors, KATP channels, and ischemic preconditioning in dogs. The American journal of physiology 264:H1327–1336. - PubMed

LinkOut - more resources