S100A9 is a functional effector of infarct wall thinning after myocardial infarction-Reference-Cited by-同舟云学术

S100A9 is a functional effector of infarct wall thinning after myocardial infarction

Published:2022-02-01 Issue:2 Volume:322 Page:H145-H155
ISSN:0363-6135
Container-title:American Journal of Physiology-Heart and Circulatory Physiology
language:en
Short-container-title:American Journal of Physiology-Heart and Circulatory Physiology

Author:

Chalise Upendra¹²,Becirovic-Agic Mediha¹²,Daseke Michael J.¹²³,Konfrst Shelby R.¹²,Rodriguez-Paar Jocelyn R.¹^ORCID,Feng Dan¹⁴,Salomon Jeffrey D.¹⁴,Anderson Daniel R.¹⁵,Cook Leah M.⁶,Lindsey Merry L.¹²^ORCID

Affiliation:

1. Department of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, Omaha, Nebraska

2. Research Service, Nebraska-Western Iowa Health Care System, Omaha, Nebraska

3. Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi

4. Division of Pediatric Critical Care, Department of Pediatrics, University of Nebraska Medical Center, Omaha, Nebraska

5. Division of Cardiovascular Medicine, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska

6. Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska

Abstract

S100A9 is a functional marker of infarct wall thinning.

Funder

American Cancer Society

Child Health Research Institute, University of Nebraska Medical Center

Svenska Sällskapet för Medicinsk Forskning

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

HHS | NIH | National Institute of General Medical Sciences

U.S. Department of Veterans Affairs

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/ajpheart.00475.2021

Reference64 articles.

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5. Exogenous IL-4 shuts off pro-inflammation in neutrophils while stimulating anti-inflammation in macrophages to induce neutrophil phagocytosis following myocardial infarction

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