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10.1161/HYPERTENSIONAHA.115.06033 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.115.06033 C4600046!4600046!26324504     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26324504&cmd=llinks): Failed to open stream: HTTP request failed! 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Haplodeficiency of Klotho Gene Causes Arterial Stiffening via Upregulation of Scleraxis Expression and Induction of Autophagy |pdf=|usr=}}{{26324504}} gab.com Text Haplodeficiency of Klotho Gene Causes Arterial Stiffening via Upregulation of Scleraxis Expression and Induction of Autophagy JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=26324504 #FOAvip The prevalence of arterial stiffness increases with age while the level of the aging-suppressor protein klotho decreases with age. The objective of this study is to assess if haplodeficiency of klotho gene causes arterial stiffness and investigate the underlying mechanism. Pulse wave velocity, a direct measure of arterial stiffness, was increased significantly in klotho heterozygous (klotho+/?) mice vs. their age-matched wild-type (WT) littermates, suggesting that haplodeficiency of klotho causes arterial stiffening. Notably, plasma aldosterone levels were elevated significantly in klotho+/? mice. Treatment with eplerenone (6 mg/kg/day, IP), an aldosterone receptor blocker, abolished klotho deficiency-induced arterial stiffening in klotho+/? mice. Klotho deficiency was associated with increased collagen and decreased elastin contents in the media of aortas. In addition, arterial MMP2, MMP9 and TGF?1 expression and myofibroblast differentiation were increased in klotho+/? mice. These klotho deficiency-related changes can be blocked by eplerenone. Protein expression of scleraxis, a transcription factor for collagen synthesis, and LC3-II/LC3-I, an index of autophagy, were upregulated in aortas of klotho+/? mice, which can be abolished by eplerenone. In cultured mouse aortic smooth muscle cells, aldosterone increased collagen-1 expression which can be completely eliminated by siRNA knockdown of scleraxis. Interestingly, alsosterone decreased elastin levels in smooth muscle cells which can be abolished by siRNA knockdown of Beclin-1, an autophagy-related gene.Conclusion: This study demonstrated for the first time that klotho deficiency-induced arterial stiffening may involve aldosterone-mediated upregulation of scleraxis and induction of autophagy which led to increased collagen-1 expression and decreased elastin levels, respectively. Twit Text FOAVip Haplodeficiency of Klotho Gene Causes Arterial Stiffening via Upregulation of Scleraxis Expression and Induction of Autophagy ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=26324504 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26324504 #FOAvip English Wikipedia <ref>{{Cite pmid|26324504}}</ref> Haplodeficiency of Klotho Gene Causes Arterial Stiffening via Upregulation of Scleraxis Expression and Induction of Autophagy #MMPMID26324504 Chen K; Zhou X; Sun Z Hypertension 2015[Nov]; 66 (5): 1006-13 PMID26324504show ga The prevalence of arterial stiffness increases with age while the level of the aging-suppressor protein klotho decreases with age. The objective of this study is to assess if haplodeficiency of klotho gene causes arterial stiffness and investigate the underlying mechanism. Pulse wave velocity, a direct measure of arterial stiffness, was increased significantly in klotho heterozygous (klotho+/?) mice vs. their age-matched wild-type (WT) littermates, suggesting that haplodeficiency of klotho causes arterial stiffening. Notably, plasma aldosterone levels were elevated significantly in klotho+/? mice. Treatment with eplerenone (6 mg/kg/day, IP), an aldosterone receptor blocker, abolished klotho deficiency-induced arterial stiffening in klotho+/? mice. Klotho deficiency was associated with increased collagen and decreased elastin contents in the media of aortas. In addition, arterial MMP2, MMP9 and TGF?1 expression and myofibroblast differentiation were increased in klotho+/? mice. These klotho deficiency-related changes can be blocked by eplerenone. Protein expression of scleraxis, a transcription factor for collagen synthesis, and LC3-II/LC3-I, an index of autophagy, were upregulated in aortas of klotho+/? mice, which can be abolished by eplerenone. In cultured mouse aortic smooth muscle cells, aldosterone increased collagen-1 expression which can be completely eliminated by siRNA knockdown of scleraxis. Interestingly, alsosterone decreased elastin levels in smooth muscle cells which can be abolished by siRNA knockdown of Beclin-1, an autophagy-related gene.Conclusion: This study demonstrated for the first time that klotho deficiency-induced arterial stiffening may involve aldosterone-mediated upregulation of scleraxis and induction of autophagy which led to increased collagen-1 expression and decreased elastin levels, respectively. äHaplodeficiency of Klotho Gene Causes Arterial Stiffening via Upregula(epmc).pdf DeepDyve Pubget Overpricing