The kidney has tremendous capacity to repair after acute injury, however, pathways guiding
adaptive and fibrotic repair are poorly understood. We developed a model of adaptive and …

After acute kidney injury (AKI), patients either recover or alternatively develop fibrosis and
chronic kidney disease. Interactions between injured epithelia, stroma, and inflammatory …

Chronic kidney disease (CKD) is estimated to affect 10–14% of global population. Kidney
fibrosis, characterized by excessive extracellular matrix deposition leading to scarring, is a …

The field of single-cell genomics and spatial technologies is rapidly evolving and has
already provided unprecedented insights into complex tissues. Major advances have been …

Overwhelming lipid peroxidation induces ferroptotic stress and ferroptosis, a nonapoptotic
form of regulated cell death that has been implicated in maladaptive renal repair in mice and …

Fibrosis, a characteristic of all chronic kidney diseases, is now recognized to be an
independent predictor of disease progression. Deposition of pathological matrix in the walls …

Kidney fibrosis is the hallmark of chronic kidney disease progression; however, at present
no antifibrotic therapies exist,–. The origin, functional heterogeneity and regulation of scar …

The year 2015 has seen great progress in the renal fibrosis field, as key studies began to
build a consensus on the importance of epithelial-to-mesenchymal transition, cell cycle …

Acute kidney injury (AKI) is considered largely reversible based on the capacity of surviving
tubular cells to dedifferentiate and replace lost cells via cell division. Here we show by …

The acutely injured mammalian kidney mounts a cellular and molecular response to repair
itself. However, in patchy regions such intrinsic processes are impaired and dysregulated …