Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Apr;35(4):321-330.
doi: 10.14670/HH-18-182. Epub 2019 Nov 6.

The regulatory role of HIF-1 in tubular epithelial cells in response to kidney injury

Yumei Qiu #  1 , Xiaowen Huang #  1 , Weichun He  2
Affiliations
Review

The regulatory role of HIF-1 in tubular epithelial cells in response to kidney injury

Yumei Qiu et al. Histol Histopathol. 2020 Apr.

Abstract

The high sensitivity to changes in oxygen tension makes kidney vulnerable to hypoxia. Both acute kidney injury and chronic kidney disease are almost always accompanied by hypoxia. Tubular epithelial cells (TECs), the dominant intrinsic cells in kidney tissue, are believed to be not only a victim in the pathological process of various kidney diseases, but also a major contributor to kidney damage. Hypoxia inducible factor-1 (HIF-1) is the main regulator of adaptive response of cells to hypoxia. Under various clinical and experimental kidney disease conditions, HIF-1 plays a pivotal role in modulating multiple cellular processes in TECs, including apoptosis, autophagy, inflammation, metabolic pattern alteration, and cell cycle arrest. A comprehensive understanding of the mechanisms by which HIF-1 regulates these cellular processes in TECs may help identify potential therapeutic targets to improve the outcome of acute kidney injury and delay the progression of chronic kidney disease.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

References

    1. Al-Bataineh M.M., Kinlough C.L., Poland P.A., Pastor-Soler N.M., Sutton T.A., Mang H.E., Bastacky S.I., Gendler S.J., Madsen C.S., Singh S., Monga S.P. and Hughey R.P. (2016). Muc1 enhances the βcatenin protective pathway during ischemia-reperfusion injury. Am. J. Physiol. Renal. Physiol. 310, F569-579. - PMC - PubMed
    1. Baek J.H., Zeng R., Weinmann-Menke J., Valerius M.T., Wada Y., Ajay A.K., Colonna M. and Kelley V.R. (2015). IL-34 mediates acute kidney injury and worsens subsequent chronic kidney disease. J. Clin. Invest. 125, 3198-3214. - PMC - PubMed
    1. Basile D.P., Donohoe D.L., Roethe K. and Mattson D.L. (2003). Chronic renal hypoxia after acute ischemic injury: effects of L-arginine on hypoxia and secondary damage. Am. J. Physiol. Renal. Physiol. 284, F338-348. - PubMed
    1. Bellot G., Garcia-Medina R., Gounon P., Chiche J., Roux D., Pouysségur J. and Mazure N.M. (2009). Hypoxia-induced autophagy is mediated through hypoxia-inducible factor induction of BNIP3 and BNIP3L via their BH3 domains. Mol. Cell Biol. 29, 2570- 2581. - PMC - PubMed
    1. Bensaad K., Favaro E., Lewis C.A., Peck B., Lord S., Collins J.M., Pinnick K.E., Wigfield S., Buffa F.M., Li J.L., Zhang Q., Wakelam M.J.O., Karpe F., Schulze A. and Harris A.L. (2014). Fatty acid uptake and lipid storage induced by HIF-1α contribute to cell growth and survival after hypoxia-reoxygenation. Cell Rep. 9, 349-365. - PubMed

Substances

LinkOut - more resources