Identifying Common Molecular Mechanisms in Experimental and Human Acute Kidney Injury
Nov 30, 2022
The McMahon lab has just published a review in Seminars in Nephrology titled “Identifying Common Molecular Mechanisms in Experimental and Human Acute Kidney Injury” (Gerhardt and McMahon). To help share this work, Elsevier provides the link below which allows free access for 50 days:
This URL provides 50 days’ free access to this article. Anyone clicking on this link before January 06, 2023 will be taken directly to the latest version of the article on ScienceDirect, which they are welcome to read or download. No sign up, registration or fees are required.
Identifying Common Molecular Mechanisms in Experimental and Human Acute Kidney Injury Louisa M.S.Gerhardt and Andrew P.McMahon Seminars in Nephrology. 2022 Nov 17. doi: 10.1016/j.semnephrol.2022.10.012. Epub ahead of print. PMID: 36402654.
Acute kidney injury (AKI) is a highly prevalent, heterogeneous syndrome, associated with increased short- and long-term mortality. A multitude of different factors cause AKI including ischemia, sepsis, nephrotoxic drugs, and urinary tract obstruction. Upon injury, the kidney initiates an intrinsic repair program that can result in adaptive repair with regeneration of damaged nephrons and functional recovery of epithelial activity, or maladaptive repair and per- sistence of damaged epithelial cells with a characteristic proinflammatory, profibrotic molecular signature. Maladap- tive repair is linked to disease progression from AKI to chronic kidney disease. Despite extensive efforts, no therapeutic strategies provide consistent benefit to AKI patients. Since kidney biopsies are rarely performed in the acute injury phase in humans, most of our understanding of AKI pathophysiology is derived from preclinical AKI models. This raises the question of how well experimental models of AKI reflect the molecular and cellular mecha- nisms underlying human AKI? Here, we provide a brief overview of available AKI models, discuss their strengths and limitations, and consider important aspects of the AKI response in mice and humans, with a particular focus on the role of proximal tubule cells in adaptive and maladaptive repair.
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