Elucidate the regulational mechanism of de-differentiation of cardiac myofibroblast in response to stretch

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K08084
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 53020:Cardiology-related
• Research Institution: Dokkyo Medical University
• Principal Investigator: Obi Syotaro 獨協医科大学, 医学部, 准教授 (10734452)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: 伸展張力

Outline of Final Research Achievements

The proriferation level and migration level decreased after human cardiac myofibroblast were exposed to stretch. The protein expression level of fibrosis marker also decreased in response to stretch. It indicates that stretch induces de-differentiation of myofibroblast. Next the knockdown of TRPV4 which was an carcium ion channel in myofibroblast did not respond to stretch. These findings indicate that one of the cause of cardiac fibrosis is the decrease of stretch, the increase of TRPV4, and the increase of fibrosis.

Free Research Field

メカノバイオロジー

Academic Significance and Societal Importance of the Research Achievements

心臓線維化の機序としてTRPV4が伸展張力に応答して線維化を制御していることが分かった。TRPV4をターゲットとした薬剤を開発することにより心臓の線維化を改善することができると期待できる。