Désirée Tampe

TL;DR: It is shown that the BMP receptor activin-like kinase 3 (Alk3) is elevated early in diseased kidneys after injury, and its deletion in the tubular epithelium leads to enhanced TGF-β1–Smad family member 3 (Smad3) signaling, epithelial damage and fibrosis, suggesting a protective role for Alk3-mediated signaling in the kidney.

TL;DR: Therapeutic concepts to inhibit or even reverse chronic kidney injury are discussed and the leading candidate antifibrotic drugs to be introduced to clinical use are reviewed.

TL;DR: It is demonstrated that CAFs exhibit a metabolic shift toward lactate and pyruvate production and fuel biosynthetic pathways of cancer cells, and their breast cancer-promoting phenotype is partly mediated by oxygen-dependent epigenetic modifications.

TL;DR: It is shown that successful inhibition of experimental kidney fibrosis through administration of BMP7 associates with normalization of Rasal1 promoter hypermethylation, and this reversal was achieved specifically through Tet3-mediated hydroxymethylation.

TL;DR: A murine model of ischemia-reperfusion injury is used to determine whether aberrant promoter methylation of RASAL1 contributes causally to the switch between physiological regeneration and tubulointerstitial fibrogenesis, a hallmark of AKI-to-CKD progression.