Latent transforming growth factor beta binding protein 4: A regulator of mitochondrial function in acute kidney injury

Recently, latent transforming growth factor beta binding protein 4 (LTBP4) was implicated in the pathogenesis of renal damage through its modulation of mitochondrial dynamics. The seminal article written by Su et al. entitled "LTBP4 (Latent Transforming Growth Factor Beta Binding Protein 4) Protects Against Renal Fibrosis via Mitochondrial and Vascular Impacts" uncovers LTBP4's renoprotective role against acute kidney injury via modulating mitochondrial dynamics. Recently, LTBP4 has emerged as a driver in the mitochondrial-dependent modulation of age-related organ pathologies. This article aims to expand our understanding of LTBP4's diverse roles in these diseases in the context of these recent findings. Neikirk et al., highlight recent findings that elucidate the findings of LTBP4 in renal damage. With increased LTBP4 expression (left), there are reductions in mitochondrial fission leading to healthy kidneys. With decreased expression (middle), increases in mitochondrial fission result in the development of chronic kidney disease. With decreased expression, however, inhibition of mitochondrial fission (right), can prevent the development of chronic kidney disease.image