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A cross talk between HIF and NF-κB in AKI

A cross talk between HIF and NF-κB in AKI Am J Physiol Renal Physiol 321: F255–F256, 2021. First published July 20, 2021; doi:10.1152/ajprenal.00256.2021 EDITORIAL 1 2,3 Zhiwen Liu and Zheng Dong Department of Nephrology, Key Laboratory of Kidney Disease and Blood Purification of Hunan Province, Second Xiangya Hospital at Central South University, Changsha, Hunan, China; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia; and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia Acute kidney injury (AKI) is manifested by a rapid decline of ureteral obstruction (UUO), or sepsis. They then showed that renal function that is associated with high morbidity and tubular Hif1a mRNA expression was strongly associated with mortality (1). However, the underlying mechanisms of AKI inflammation, highlighting the possible connection between remain poorly understood, and effective treatment for AKI is tubular HIF-1a and inflammation in AKI. They further con- unavailable. Both hypoxia-inducible factor (HIF) and NF-κB ducted a series of in vivo and in vitro experiments, leading to have been implicated in gene regulation in AKI, but very lit- the finding that NF-κB may transcriptionally regulate HIF-1a tle is known about their cross talk. in renal tubule cells. Notably, their chromatin immunopreci- Renal tubular cells are high in oxygen consumption. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Physiology-Renal Physiology The American Physiological Society

A cross talk between HIF and NF-κB in AKI

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ISSN
1931-857x
eISSN
1522-1466
DOI
10.1152/ajprenal.00256.2021
Publisher site
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Abstract

Am J Physiol Renal Physiol 321: F255–F256, 2021. First published July 20, 2021; doi:10.1152/ajprenal.00256.2021 EDITORIAL 1 2,3 Zhiwen Liu and Zheng Dong Department of Nephrology, Key Laboratory of Kidney Disease and Blood Purification of Hunan Province, Second Xiangya Hospital at Central South University, Changsha, Hunan, China; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia; and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia Acute kidney injury (AKI) is manifested by a rapid decline of ureteral obstruction (UUO), or sepsis. They then showed that renal function that is associated with high morbidity and tubular Hif1a mRNA expression was strongly associated with mortality (1). However, the underlying mechanisms of AKI inflammation, highlighting the possible connection between remain poorly understood, and effective treatment for AKI is tubular HIF-1a and inflammation in AKI. They further con- unavailable. Both hypoxia-inducible factor (HIF) and NF-κB ducted a series of in vivo and in vitro experiments, leading to have been implicated in gene regulation in AKI, but very lit- the finding that NF-κB may transcriptionally regulate HIF-1a tle is known about their cross talk. in renal tubule cells. Notably, their chromatin immunopreci- Renal tubular cells are high in oxygen consumption.

Journal

American Journal of Physiology-Renal Physiology – The American Physiological Society

Published: Sep 1, 2021

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