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      Sex hormones and sex chromosomes cause sex differences in the development of cardiovascular diseases

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          Abstract

          This review summarizes recent evidence concerning hormonal and sex chromosome effects in obesity, atherosclerosis, aneurysms, ischemia/reperfusion injury, and hypertension. Cardiovascular diseases (CVD) occur and progress differently in the two sexes, because biological factors differing between the sexes have sex-specific protective and harmful effects. By comparing the two sexes directly, and breaking down sex into its component parts, one can discover sex-biasing protective mechanisms that might be targeted in the clinic. Gonadal hormones, especially estrogens and androgens, have long been found to account for some sex differences in CVD, and molecular mechanisms mediating these effects have recently been elucidated. More recently the inherent sexual inequalities in effects of sex chromosome genes have also been implicated as contributors in animal models of CVDs, especially a deleterious effect of the second X chromosome found in females but not in males. Hormonal and sex chromosome mechanisms interact in the sex-specific control of certain diseases, sometimes by opposing the action of the other.

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          Author and article information

          Journal
          9505803
          8623
          Arterioscler Thromb Vasc Biol
          Arterioscler. Thromb. Vasc. Biol.
          Arteriosclerosis, thrombosis, and vascular biology
          1079-5642
          1524-4636
          27 March 2017
          09 March 2017
          May 2017
          01 May 2018
          : 37
          : 5
          : 746-756
          Affiliations
          Department of Integrative Biology & Physiology, University of California, Los Angeles CA (A.P.A.); Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington KY (L.A.C.); Department of Anesthesiology (M.E.) and Department of Human Genetics (K.R.), David Geffen School of Medicine at UCLA, Los Angeles CA; and Department of Medicine, Georgetown University Medical Center, Washington DC (K.S.)
          Author notes
          Correspondence: Arthur P. Arnold, Department of Integrative Biology & Physiology, UCLA, arnold@ 123456ucla.edu , 310-825-2169
          Article
          PMC5437981 PMC5437981 5437981 nihpa855049
          10.1161/ATVBAHA.116.307301
          5437981
          28279969
          4c3b1ea7-fa93-4872-a9d8-bc397421bbee
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