The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Sepsis-induced acute kidney injury
Open accessAbstract
Purpose of review: Sepsis is a common and frequently fatal condition in which mortality has been consistently linked to increasing organ dysfunction. For example, acute kidney injury (AKI) occurs in 40–50% of septic patients and increases mortality six to eight-fold. However, the mechanisms by which sepsis causes organ dysfunction are not well understood and hence current therapy remains reactive and nonspecific. Recent findings: Recent studies have challenged the previous notion that organ dysfunction is solely secondary to hypoperfusion, by showing, for example, that AKI occurs in the setting of normal or increased renal blood flow; and that it is characterized not by acute tubular necrosis or apoptosis, but rather by heterogeneous areas of colocalized sluggish peritubular blood flow and tubular epithelial cell oxidative stress. Evidence has also shown that microvascular dysfunction, inflammation, and the metabolic response to inflammatory injury are fundamental pathophysiologic mechanisms that may explain the development of sepsis-induced AKI. Summary: The implications of these findings are significant because in the context of decades of negative clinical trials in the field, the recognition that other mechanisms are at play opens the possibility to better understand the processes of injury and repair, and provides an invaluable opportunity to design mechanism-targeted therapeutic interventions.
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Cites
Autophagy fights disease through cellular self-digestion
Mizushima, N., Levine, B., Cuervo, A. M., & Klionsky, D. J. (2008) · Nature · doi:10.1038/nature06639 · Cited by 6,452
Kang, H. M., Ahn, S. H., Choi, P., Ko, Y.-A., Han, S. H., Chinga, F., Park, A. S. D., Tao, J., Sharma, K., Pullman, J., et al. (2015) · Nature Medicine · doi:10.1038/nm.3762 · Cited by 1,555
The CD28 Signaling Pathway Regulates Glucose Metabolism
Frauwirth, K. A., Riley, J. L., Harris, M. H., Parry, R. V., Rathmell, J. C., Plas, D. R., Elstrom, R. L., June, C. H., & Thompson, C. B. (2002) · Immunity · doi:10.1016/s1074-7613(02)00323-0 · Cited by 1,475
Mitochondria and the Autophagy–Inflammation–Cell Death Axis in Organismal Aging
Green, D. R., Galluzzi, L., & Kroemer, G. (2011) · Science · doi:10.1126/science.1201940 · Cited by 1,245
High versus low blood-pressure target in patients with septic shock.
Asfar, P., Meziani, F., Hamel, J.-F., Grelon, F., Megarbane, B., Anguel, N., Mira, J.-P., Dequin, P.-F., Gergaud, S., Weiss, N., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1312173 · Cited by 1,239
Augmenting Autophagy to Treat Acute Kidney Injury during Endotoxemia in Mice
Howell, G. M., Gomez, H., Collage, R. D., Loughran, P., Zhang, X., Escobar, D. A., Billiar, T. R., Zuckerbraun, B. S., & Rosengart, M. R. (2013) · PLoS ONE · doi:10.1371/journal.pone.0069520 · Cited by 105
Cited by
Ronco, C., Bellomo, R., & Kellum, J. A. (2019) · The Lancet · doi:10.1016/s0140-6736(19)32563-2 · Cited by 1,910
Self-citationBlood 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
Gut–kidney crosstalk in septic acute kidney injury
Zhang, J., Ankawi, G., Sun, J., Digvijay, K., Yin, Y., Rosner, M. H., & Ronco, C. (2018) · Critical Care · doi:10.1186/s13054-018-2040-y · Cited by 95
miR-129-5p alleviates LPS-induced acute kidney injury via targeting HMGB1/TLRs/NF-kappaB pathway
Huang, X., Hou, X., Chuan, L., Wei, S., Wang, J., Yang, X., & Ru, J. (2020) · International Immunopharmacology · doi:10.1016/j.intimp.2020.107016 · Cited by 47
Ye, J., Feng, H., & Peng, Z. (2022) · Brazilian Journal of Medical and Biological Research · doi:10.1590/1414-431x2021e11571 · Cited by 17
Metadata
- Authors
- Gómez, H., & Kellum, J. A.
- Venue
- Current Opinion in Critical Care
- Published
- 2016-12
- Volume
- 22
- Issue
- 6
- Pages
- 546-553
- ISSN
- 1070-5295 (ISSN-L)
- 1531-7072
- OpenAlex
- W2181632327
- Cited by
- 312
- References
- 6
- FWCI
- 15.08
- Type
- journal article
- Language
- en
- Open access
- green
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