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. 2021 Jun 22;12:662020. doi: 10.3389/fphar.2021.662020

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Copyright © 2021 Marquez-Exposito, Tejedor-Santamaria, Santos-Sanchez, Valentijn, Cantero-Navarro, Rayego-Mateos, Rodrigues-Diez, Tejera-Muñoz, Marchant, Sanz, Ortiz, Goldschmeding and Ruiz-Ortega.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed mechanisms involved in aging-related FA-AKI increased susceptibility. In response to FA injury, aging kidneys present an increase of KIM-1 expression, indicator of tubular damage, lower levels of nephroprotective factors and immunosenescent infiltrating cells. The tubular cell damage can be lethal; in FA-aging kidneys there is an activation of inflammatory forms of cell death, such as necroptosis and ferroptosis, as well as an inhibition of apoptosis. In aging kidneys, injured tubular cells change their phenotype to a proinflammatory and senescent one, being IL-6 one of the most upregulated cytokines. These cellular and molecular changes may partially underlie the age-related increased susceptibility to developing more severe AKI in response to FA.