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In this study, we evaluated the roles of\n                      <jats:italic>miR<\/jats:italic>\n                      \u2010\n                      <jats:italic>145<\/jats:italic>\n                      in VSMCs subjected to mechanical stretching in aortic dissection (AD).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The expression of miR\u2010145 in the aortic vessel wall of model animals and patients with AD was analyzed by quantitative polymerase chain reaction. miR\u2010145\u2010related protein\u2010protein interaction networks and Wikipathways were used to analyze VSMC phenotypic transformation pathways regulated by miR\u2010145. We used gain\u2010 and loss\u2010of\u2010function studies to evaluate the effects of miR\u2010145 on VSMC differentiation under mechanical stretch induction and assessed whether Kr\u00fcppel\u2010like factor 4 (KLF4) was regulated by miR\u2010145 in the aorta under mechanical stretch conditions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>miR<\/jats:italic>\n                      \u2010\n                      <jats:italic>145<\/jats:italic>\n                      was abundantly expressed in the walls of the normal human aorta, but was significantly downregulated in animal models and the walls of patients with dissection. We found that contractile phenotype\u2010related proteins were downregulated in VSMCs subjected to mechanical stretching, whereas the expression of secreted phenotype\u2010related proteins increased.\n                      <jats:italic>miR<\/jats:italic>\n                      \u2010\n                      <jats:italic>145<\/jats:italic>\n                      overexpression also downregulated contractile phenotype\u2010related proteins in VSMCs and suppressed upregulation of phenotype\u2010related proteins. Finally, under mechanical stretching, KLF4 expression was significantly increased in VSMCs, and overexpression of\n                      <jats:italic>miR<\/jats:italic>\n                      \u2010\n                      <jats:italic>145<\/jats:italic>\n                      blocked this effect.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Our results confirmed that mechanical stretch\u2010induced phenotypic transformation of VSMCs to promote AD via upregulation of KLF4; this mechanism was regulated by\n                      <jats:italic>miR<\/jats:italic>\n                      \u2010\n                      <jats:italic>145<\/jats:italic>\n                      , which directly modulated KLF4 expression and VSMC differentiation.\n                    <\/jats:p>\n                  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