Decreasing mitochondrial fission diminishes vascular smooth muscle cell migration and ameliorates intimal hyperplasia
Author(s) -
Li Wang,
Tianzheng Yu,
Hakjoo Lee,
Dawn K. O'Brien,
Hiromi Sesaki,
Yisang Yoon
Publication year - 2015
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvv005
Subject(s) - mitochondrial fission , microbiology and biotechnology , intimal hyperplasia , mfn2 , vascular smooth muscle , mitochondrial fusion , mitochondrion , biology , chemistry , mitochondrial dna , endocrinology , biochemistry , smooth muscle , gene
Vascular smooth muscle cell (VSMC) migration in response to arterial wall injury is a critical process in the development of intimal hyperplasia. Cell migration is an energy-demanding process that is predicted to require mitochondrial function. Mitochondria are morphologically dynamic, undergoing continuous shape change through fission and fusion. However, the role of mitochondrial morphology in VSMC migration is not well understood. The aim of the study is to understand how mitochondrial fission contributes to VSMC migration and provides its in vivo relevance in the mouse model of intimal hyperplasia.
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