Toxic effects of cell-free hemoglobin on the microvascular endothelium: implications for pulmonary and nonpulmonary organ dysfunction-Reference-Cited by-同舟云学术

Toxic effects of cell-free hemoglobin on the microvascular endothelium: implications for pulmonary and nonpulmonary organ dysfunction

Published:2021-08-01 Issue:2 Volume:321 Page:L429-L439
ISSN:1040-0605
Container-title:American Journal of Physiology-Lung Cellular and Molecular Physiology
language:en
Short-container-title:American Journal of Physiology-Lung Cellular and Molecular Physiology

Author:

Meegan Jamie E.¹^ORCID,Bastarache Julie A.¹²³^ORCID,Ware Lorraine B.¹²

Affiliation:

1. Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee

2. Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee

3. Department of Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, Tennessee

Abstract

Levels of circulating cell-free hemoglobin are elevated during hemolytic and inflammatory diseases and contribute to organ dysfunction and severity of illness. Though several studies have investigated the contribution of hemoglobin to tissue injury, the precise signaling mechanisms of hemoglobin-mediated endothelial dysfunction in the lung and other organs are not yet completely understood. The purpose of this review is to highlight the knowledge gained thus far and the need for further investigation regarding hemoglobin-mediated endothelial inflammation and injury to develop novel therapeutic strategies targeting the damaging effects of cell-free hemoglobin.

Funder

HHS | NIH | National Heart, Lung, and Blood Institute

Publisher

American Physiological Society

Subject

Cell Biology,Physiology (medical),Pulmonary and Respiratory Medicine,Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/ajplung.00018.2021

Reference103 articles.

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3. Intravascular Hemolysis, Vascular Endothelial Cell Activation and Thrombophilia in Splenectomized Patients with Hemoglobin E/β-Thalassemia Disease

4. Nitric Oxide Scavenging by Red Blood Cell Microparticles and Cell-Free Hemoglobin as a Mechanism for the Red Cell Storage Lesion

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