Renoprotective and Immunomodulatory Effects of GDF15 following AKI Invoked by Ischemia-Reperfusion Injury.

Background: encodes a TGF- superfamily member that is rapidly activated in response to stress in multiple organ systems, including the kidney. However, there has been a lack of information about activity and effects in normal kidney and in AKI.

Methods: We used genome editing to generate a mouse line, removing at the targeted allele, and enabling direct visualization and genetic modification of -expressing cells.

Single-Cell Profiling Reveals Sex, Lineage, and Regional Diversity in the Mouse Kidney.

Chronic kidney disease affects 10% of the population with notable differences in ethnic and sex-related susceptibility to kidney injury and disease. Kidney dysfunction leads to significant morbidity and mortality and chronic disease in other organ systems. A mouse-organ-centered understanding underlies rapid progress in human disease modeling and cellular approaches to repair damaged systems.

Molecular characterization of the transition from acute to chronic kidney injury following ischemia/reperfusion.

Though an acute kidney injury (AKI) episode is associated with an increased risk of chronic kidney disease (CKD), the mechanisms determining the transition from acute to irreversible chronic injury are not well understood. To extend our understanding of renal repair, and its limits, we performed a detailed molecular characterization of a murine ischemia/reperfusion injury (IRI) model for 12 months after injury. Together, the data comprising RNA-sequencing (RNA-seq) analysis at multiple time points, histological studies, and molecular and cellular characterization of targeted gene activity provide a comprehensive profile of injury, repair, and long-term maladaptive responses following IRI.