Jonay Poveda

TL;DR: It is shown that ferrostatin-1 (Fer-1), an inhibitor of ferroptosis, preserved renal function and decreased histologic injury, oxidative stress, and tubular cell death in this model, and that immunogenicity secondary to ferroPTosis may further worsen the damage, although necroptosis-related proteins may have additional roles in AKI.

TL;DR: Despite initial cell culture and clinical trials results supporting the renal safety of tenofovir, its clinical use is associated with a low, albeit significant, risk of kidney injury, and regular monitoring of proximal tubular dysfunction and serum creatinine in high-risk patients is required to minimize nephrotoxicity.

TL;DR: A correct understanding of these interactions may lead to the design of novel therapeutic approaches to CKD and CKD-related inflammatory and ageing features as well as to inflammation/ageing in general.

TL;DR: The morphological and functional mitochondrial changes during AKI are reviewed, as well as changes in the expression of mitochondrial genes and proteins, and the current status of novel therapeutic strategies specifically targeting mitochondria are summarized.

TL;DR: While research into epigenetic modulators may provide novel therapies for kidney disease, caution should be exercised based on the clinical nephrotoxicity of some drugs.