HMGB1 Turns Renal Tubular Epithelial Cells into Inflammatory Promoters by Interacting with TLR4 During Sepsis-Reference-Cited by-同舟云学术

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HMGB1 Turns Renal Tubular Epithelial Cells into Inflammatory Promoters by Interacting with TLR4 During Sepsis

Published:2016-01 Issue:1 Volume:36 Page:9-19
ISSN:1079-9907
Container-title:Journal of Interferon & Cytokine Research
language:en
Short-container-title:Journal of Interferon & Cytokine Research

Author:

Zheng Shixiang¹,Pan Yangbin¹²,Wang Cairong³,Liu Yipeng⁴,Shi Ming¹,Ding Guohua¹

Affiliation:

1. Division of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.

2. Department of OB/GYN and Women's Health, School of Medicine, University of Louisville, Louisville, Kentucky.

3. Division of Critical Care Medicine, Union Hospital of Fujian Medical University, Fuzhou, Fujian, China.

4. Department of Nephrology, Qianfoshan Hospital, Shandong University, Jinan, Shangdong, China.

Publisher

Mary Ann Liebert Inc

Subject

Virology,Cell Biology,Immunology

Link

http://www.liebertpub.com/doi/pdf/10.1089/jir.2015.0067

Reference37 articles.

1. Urine levels of HMGB1 in Systemic Lupus Erythematosus patients with and without renal manifestations

2. HMGB1 Is a Therapeutic Target for Sterile Inflammation and Infection

3. Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome, and associated costs of care

4. Validation of Cell-Cycle Arrest Biomarkers for Acute Kidney Injury Using Clinical Adjudication

5. p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes

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3. Targeting HMGB1: A Potential Therapeutic Strategy for Chronic Kidney Disease;International Journal of Biological Sciences;2023

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5. Suppression of lncRNA GAS6-AS2 alleviates sepsis-related acute kidney injury through regulating the miR-136-5p/OXSR1 axis in vitro and in vivo;Renal Failure;2022-07-06

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