Long-term graft survival after kidney transplantation remains unsatisfactory and
unpredictable. Interstitial fibrosis and tubular atrophy are major contributors to late graft loss;
features of tubular cell senescence, such as increased p16 INK4a expression, associate
with these tubulointerstitial changes, but it is unknown whether the relationship is causal.
Here, loss of the INK4a locus in mice, which allows escape from p16 INK4a-dependent
senescence, significantly reduced interstitial fibrosis and tubular atrophy and associated …