E. Kefaloyianni

This study shows that acute kidney injury (AKI) increases circulating TNFR1/2 levels, which correlate with kidney injury severity and progression to fibrosis, particularly through extracellular vesicle-bound forms.

This study identifies osteopontin (OPN) released by injured kidneys as a mediator of acute lung injury, showing its role in causing pulmonary inflammation and edema.

This study shows that TNF inhibition with etanercept prevents AKI-to-CKD transition and fibrosis as effectively as EGFR inhibition in mice, suggesting TNF as a downstream effector of EGFR-driven profibrotic signals.