The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Acute Kidney Injury
Open accessAbstract
Acute kidney injury (AKI) is a global public health concern associated with high morbidity, mortality, and healthcare costs. Other than dialysis, no therapeutic interventions reliably improve survival, limit injury, or speed recovery. Despite recognized shortcomings of in vivo animal models, the underlying pathophysiology of AKI and its consequence, chronic kidney disease (CKD), is rich with biological targets. We review recent findings relating to the renal vasculature and cellular stress responses, primarily the intersection of the unfolded protein response, mitochondrial dysfunction, autophagy, and the innate immune response. Maladaptive repair mechanisms that persist following the acute phase promote inflammation and fibrosis in the chronic phase. Here macrophages, growth-arrested tubular epithelial cells, the endothelium, and surrounding pericytes are key players in the progression to chronic disease. Better understanding of these complex interacting pathophysiological mechanisms, their relative importance in humans, and the utility of biomarkers will lead to therapeutic strategies to prevent and treat AKI or impede progression to CKD or end-stage renal disease (ESRD).
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Cites
The eIF2α/ATF4 pathway is essential for stress-induced autophagy gene expression
B’chir, W., Maurin, A.-C., Carraro, V., Averous, J., Jousse, C., Muranishi, Y., Parry, L., Stepien, G., Fafournoux, P., & Bruhat, A. (2013) · Nucleic Acids Research · doi:10.1093/nar/gkt563 · Cited by 1,162
UPR, autophagy, and mitochondria crosstalk underlies the ER stress response
Senft, D., & Ronai, Z. A. (2015) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2015.01.002 · Cited by 1,121
Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models
Brooks, C., Wei, Q., Cho, S.-G., & Dong, Z. (2009) · Journal of Clinical Investigation · doi:10.1172/jci37829 · Cited by 735 · cited 2×
“Pharmacological inhibition of Drp1—a fission protein that constricts and cleaves mitochondria, leading to fragmentation— reduces mitochondrial damage, cytochrome c release, apoptosis, and renal injury (31).”
BackgroundDent, C. L., Ma, Q., Dastrala, S., Bennett, M., Mitsnefes, M. M., Barasch, J., & Devarajan, P. (2007) · Critical Care · doi:10.1186/cc6192 · Cited by 483
Cited by
Activation of BNIP3-mediated mitophagy protects against renal ischemia–reperfusion injury
Tang, C., Han, H., Liu, Z., Liu, Y., Yin, L., Cai, J., He, L., Liu, Y., Chen, G., Zhang, Z., et al. (2019) · Cell Death & Disease · doi:10.1038/s41419-019-1899-0 · Cited by 219
Blood platelets and sepsis pathophysiology: A new therapeutic prospect in critical ill patients?
Dewitte, A., Lepreux, S., Villeneuve, J., Rigothier, C., Combe, C., Ouattara, A., & Ripoche, J. (2017) · Annals of Intensive Care · doi:10.1186/s13613-017-0337-7 · Cited by 194
Barrera-Chimal, J., Estrela, G. R., Lechner, S. M., Giraud, S., El Moghrabi, S., Kaaki, S., Kolkhof, P., Hauet, T., & Jaisser, F. (2018) · Kidney International · doi:10.1016/j.kint.2017.12.016 · Cited by 183
Proximal tubule ATR regulates DNA repair to prevent maladaptive renal injury responses
Kishi, S., Brooks, C. R., Taguchi, K., Ichimura, T., Mori, Y., Akinfolarin, A., Gupta, N., Galichon, P., Elias, B. C., Suzuki, T., et al. (2019) · Journal of Clinical Investigation · doi:10.1172/jci122313 · Cited by 117
Self-citationFoxO3 activation in hypoxic tubules prevents chronic kidney disease
Li, L., Kang, H., Zhang, Q., D’Agati, V. D., Al-Awqati, Q., & Lin, F. (2019) · Journal of Clinical Investigation · doi:10.1172/jci122256 · Cited by 105
Metadata
- Authors
- Zuk, A., & Bonventre, J. V.
- Venue
- Annual Review of Medicine
- Publisher
- Annual Reviews
- Published
- 2016-01-14
- Volume
- 67
- Issue
- 1
- Pages
- 293-307
- ISSN
- 0066-4219 (ISSN-L)
- 1545-326X
- OpenAlex
- W2233632661
- Cited by
- 739
- References
- 4
- FWCI
- 12.18
- Type
- journal article
- Language
- en
- Open access
- bronze
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