The anti-Thy-1.1 model is a rat model of mesangial proliferative glomerulonephritis characterized by initial mesangiolysis followed by mesangial cell proliferation and accumulation of mesangial matrix with subsequent resolution and the return to almost normal histology. In this review we discuss the pathogenesis of the initial injury, the mechanisms governing mesangial cell proliferation and matrix expansion, and some of the processes involved in the resolution of glomerular injury. Understanding these processes of mesangial cell injury and recovery may provide insights into the pathogenesis of human mesangial cell diseases such as IgA nephropathy.