Publications by authors named "Takanori Hironaka"
Article Synopsis
- Myofibroblasts contribute to tissue fibrosis by producing collagen, but the molecular mechanisms behind their collagen production are not well understood.
- The study identifies VGLL3, a protein expressed in myofibroblasts from fibrotic hearts, as a key player that enhances collagen production through a series of molecular interactions.
- Findings suggest that targeting VGLL3 could offer a new therapeutic approach to mitigate tissue fibrosis, especially after heart injury like myocardial infarction.
Fibrosis is mainly triggered by inflammation in various tissues, such as heart and liver tissues, and eventually leads to their subsequent dysfunction. Fibrosis is characterized by the excessive accumulation of extracellular matrix proteins (e.g.
View Article and Find Full Text PDFFibrosis is a condition characterized by the overproduction of extracellular matrix (ECM) components (e.g., collagen) in the myofibroblasts, causing tissue hardening and eventual organ dysfunction.
View Article and Find Full Text PDFQuantitative whole-body autoradiography (QWBA) is largely used to evaluate tissue distribution of small molecule drugs. In QWBA, radioactivity is measured as the intensity obtained from the autoradiogram. It is known that lower intensity per a region of interest (ROI) or smaller size of ROI increases the variability of intensity.
View Article and Find Full Text PDFFibrosis is attributed to excess deposition of extracellular matrix (ECM) proteins including collagen and is associated with various organ dysfunction. This excessive ECM is produced by myofibroblasts, which are differentiated from various cells by a variety of stimuli, represented by TGF-β. However, molecular mechanisms for the regulation of ECM production in myofibroblasts remain obscure.
View Article and Find Full Text PDFPurpose: PEPT1 mediates the intestinal absorption of many drugs, but its contribution to oral absorption of drugs is still controversial. The objective of this study is to quantitatively evaluate the contribution of PEPT1 to oral absorption of cephalexin, a typical substrate for PEPT1, in rats.
Materials And Methods: The absorbability of cephalexin via PEPT1 or passive diffusion was assessed in five intestinal segments by utilizing glycyl-proline as a competitive inhibitor by in-situ closed loop method.