Hitoshi Yoshiji

TL;DR: The main aim of this article is to review recent literature on TIMPs with special emphasis on their biological activities and the possibility that they may have paradoxical roles in tumor progression.

TL;DR: The results suggested that the RAS, especially AT‐II and AT1‐R interaction plays a pivotal role in liver fibrosis development through HSC activation, and both CA and PE may provide an effective new strategy for anti–liver fibrosis therapy.

TL;DR: Transgenic mice overexpressing human TIMP‐1 in the liver under control of the albumin promoter/enhancer suggest that TIMP•1 does not by itself result in liver fibrosis, but strongly promotes Liver fibrosis development.

TL;DR: Combining the blockade of PD‐1 and VEGFR2 induced a synergistic in‐vivo anti‐tumour effect, possibly through different mechanisms that might not be mutually exclusive.

TL;DR: TIMP‐1 significantly attenuated spontaneous resolution of liver fibrosis by the combination of a net reduction of the MMP activity and suppression of apoptosis in HSC.