Journal
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 39, Issue 12, Pages E247-E252Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.119.312581
Keywords
atherosclerosis; catenin; macrophage; myocardial infarction; vascular remodeling
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Funding
- National Institutes of Health [HL123302, HL119053, HL135854, HL147313]
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SMC phenotypic transition-triggered arterial remodeling is a hallmark process that follows vascular injury. Recent identification of the important regulators and signaling pathways involved in this process is likely to provide novel insights into the disease development, which may lead to new therapeutic strategies in the prevention and treatment of proliferative vascular diseases. Due to divergent biological factors causing sexspecific protective and harmful effects between males and females, many cardiovascular diseases show milder phenotypes in females than in males in their young ages. Thus, most studies on vascular remodeling have been performed in only one sex, mainly on males. This is partially due to the lack of SMC-specific Cre mouse lines for both males and females in recent years. However, National Institutes of Health guidelines requires researchers to consider sex difference as a biological variable in preclinical animal studies. ATVB has also published several articles to emphasize the importance of studying and reporting sex and sex difference.(59-62) Therefore, it is suggested to include both males and females in designing, executing, and reporting experiments studying SMC phenotypes in vascular remodeling and other related arterial pathology. Development of SMC- specific Cre lines that can cause Cre-Lox recombination in both male and female mice is likely to enhance the study of SMC phenotypes in vascular remodeling and related pathology in females.(63)
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