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Hernández-Reséndiz S, Muñoz-Vega M, Contreras WE, et al. Responses of Endothelial Cells Towards Ischemic Conditioning Following Acute Myocardial Infarction. Cond Med. 2018;1(5):247-258
Hernández-Reséndiz, S., Muñoz-Vega, M., Contreras, W. E., Crespo-Avilan, G. E., Rodriguez-Montesinos, J., Arias-Carrión, O., Pérez-Méndez, O., Boisvert, W. A., Preissner, K. T., & Cabrera-Fuentes, H. A. (2018). Responses of Endothelial Cells Towards Ischemic Conditioning Following Acute Myocardial Infarction. Conditioning medicine, 1(5), 247-258.
Hernández-Reséndiz, Sauri, et al. "Responses of Endothelial Cells Towards Ischemic Conditioning Following Acute Myocardial Infarction." Conditioning medicine vol. 1,5 (2018): 247-258.
Hernández-Reséndiz S, Muñoz-Vega M, Contreras WE, Crespo-Avilan GE, Rodriguez-Montesinos J, Arias-Carrión O, Pérez-Méndez O, Boisvert WA, Preissner KT, Cabrera-Fuentes HA. Responses of Endothelial Cells Towards Ischemic Conditioning Following Acute Myocardial Infarction. Cond Med. 2018 Aug;1(5):247-258. PMID: 30338315; PMCID: PMC6191189.
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Cond Med. 2018 Aug;1(5):247-258.

Responses of Endothelial Cells Towards Ischemic Conditioning Following Acute Myocardial Infarction.

Conditioning medicine

Sauri Hernández-Reséndiz, Mónica Muñoz-Vega, Whendy E Contreras, Gustavo E Crespo-Avilan, Julian Rodriguez-Montesinos, Oscar Arias-Carrión, Oscar Pérez-Méndez, William A Boisvert, Klaus T Preissner, Hector A Cabrera-Fuentes

Affiliations

  1. Cardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore, Singapore.
  2. National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore.
  3. Escuela de Ingeniería y Ciencias, Centro de Biotecnología-FEMSA, Tecnológico de Monterrey, Monterrey, NL, México.
  4. Unidad de Trastornos del Movimiento y Sueño, Hospital General Dr. Manuel Gea González. Ciudad de México, México.
  5. Institute of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany.
  6. Molecular Biology Department, Instituto Nacional de Cardiología "Ignacio Chávez", C.D de México, México.
  7. Kazan Federal University, Department of Microbiology, Kazan, Russian Federation.
  8. Center for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Hawaii, USA.

PMID: 30338315 PMCID: PMC6191189

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

Conflict of interest statement

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

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