The DOI matches its Crossref record; 145 of the 145 references it cites were found in a registry or an index.
Hypoxia as a key player in the AKI-to-CKD transition
Abstract
Recent clinical and animal studies have shown that acute kidney injury (AKI), even if followed by complete recovery of renal function, can eventually result in chronic kidney disease (CKD). Renal hypoxia is emerging as a key player in the pathophysiology of the AKI-to-CKD transition. Capillary rarefaction after AKI episodes induces renal hypoxia, which can in turn profoundly affect tubular epithelial cells, (myo)fibroblasts, and inflammatory cells, culminating in tubulointerstitial fibrosis, i.e., progression to CKD. Damaged tubular epithelial cells that fail to redifferentiate might supply a decreased amount of vascular endothelial growth factor and contribute to capillary rarefaction, thus aggravating hypoxia and forming a vicious cycle. Mounting evidence also shows that epigenetic changes are closely related to renal hypoxia in the pathophysiology of CKD progression. Animal experiments suggest that targeting hypoxia is a promising strategy to block the transition from AKI to CKD. However, the precise mechanisms by which hypoxia induces the AKI-to-CKD transition and by which hypoxia-inducible factor activation can exert a protective effect in this context should be clarified in further studies.
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Cellular and developmental control of O 2 homeostasis by hypoxia-inducible factor 1α
Iyer, N. V., Kotch, L. E., Agani, F., Leung, S. W., Laughner, E., Wenger, R. H., Gassmann, M., Gearhart, J. D., Lawler, A. M., Yu, A. Y., et al. (1998) · Genes & Development · doi:10.1101/gad.12.2.149 · Cited by 2,476
Chronic kidney disease after acute kidney injury: a systematic review and meta-analysis
Coca, S. G., Singanamala, S., & Parikh, C. R. (2012) · Kidney International · doi:10.1038/ki.2011.379 · Cited by 2,256
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Bonventre, J. V., & Yang, L. (2011) · Journal of Clinical Investigation · doi:10.1172/jci45161 · Cited by 2,019
VEGF Inhibition and Renal Thrombotic Microangiopathy
Eremina, V., Jefferson, J. A., Kowalewska, J., Hochster, H., Haas, M., Weisstuch, J., Richardson, C., Kopp, J. B., Kabir, M. G., Backx, P. H., et al. (2008) · New England Journal of Medicine · doi:10.1056/nejmoa0707330 · Cited by 1,504
Fate Tracing Reveals the Pericyte and Not Epithelial Origin of Myofibroblasts in Kidney Fibrosis
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Origin and function of myofibroblasts in kidney fibrosis
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Cited by
Immune cells and inflammation in AKI to CKD progression
Sato, Y., & Yanagita, M. (2018) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00195.2018 · Cited by 273
Li, S., Lin, Q., Shao, X., Zhu, X., Wu, J., Wu, B., Zhang, M., Zhou, W., Zhou, Y., Jin, H., et al. (2020) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2019.12.005 · Cited by 112
Lee, J., Lee, J., Kim, K., Lee, J., Jung, Y., Hyeon, J. S., Seo, A., Jin, W., Weon, B., Shin, N., et al. (2024) · Kidney International · doi:10.1016/j.kint.2024.01.040 · Cited by 76
Hypoxia and its Emerging Therapeutics in Neurodegenerative, Inflammatory and Renal Diseases
Bhatia, D., Ardekani, M. S., Shi, Q., & Movafagh, S. (2017) · Hypoxia and Human Diseases · doi:10.5772/66089 · Cited by 17
Metadata
- Authors
- Tanaka, S., Tanaka, T., & Nangaku, M.
- Venue
- American Journal of Physiology-Renal Physiology
- Publisher
- American Physiological Society
- Published
- 2014-12-01
- Volume
- 307
- Issue
- 11
- Pages
- F1187-F1195
- ISSN
- 1522-1466 (ISSN-L)
- 1931-857X
- OpenAlex
- W1969312511
- Cited by
- 280
- References
- 145
- FWCI
- 10.27
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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