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10.1038/s41467-018-04994-z http://scihub22266oqcxt.onion/10.1038/s41467-018-04994-z C6028646!6028646!29967491     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2018 ; 9 (ä): ä Nephropedia Template TP {{tp|p=29967491|t=2018. TGF-? signaling alters H4K20me3 status via miR-29 and contributes to cellular senescence and cardiac aging |pdf=|usr=}}{{29967491}} gab.com Text TGF- signaling alters H4K20me3 status via miR-29 and contributes to cellular senescence and cardiac aging JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29967491 #FOAvip Cellular senescence is a well-orchestrated programmed process involved in age-related pathologies, tumor suppression and embryonic development. TGF-?/Smad is one of the predominant pathways that regulate damage-induced and developmentally programmed senescence. Here we show that canonical TGF-? signaling promotes senescence via miR-29-induced loss of H4K20me3. Mechanistically, oxidative stress triggers TGF-? signaling. Activated TGF-? signaling gives rise to acute accumulation of miR-29a and miR-29c, both of which directly suppress their novel target, Suv4-20h, thus reducing H4K20me3 abundance in a Smad-dependent manner, which compromises DNA damage repair and genome maintenance. Loss of H4K20me3 mediated by the senescent TGF-?/miR-29 pathway contributes to cardiac aging in vivo. Disruption of TGF-? signaling restores H4K20me3 and improves cardiac function in aged mice. Our study highlights the sequential mechanisms underlying the regulation of senescence, from senescence-inducing triggers to activation of responsive signaling followed by specific epigenetic alterations, shedding light on potential therapeutic interventions in cardiac aging. Twit Text FOAVip TGF- signaling alters H4K20me3 status via miR-29 and contributes to cellular senescence and cardiac aging ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29967491 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29967491 #FOAvip English Wikipedia <ref>{{Cite pmid|29967491}}</ref> TGF-? signaling alters H4K20me3 status via miR-29 and contributes to cellular senescence and cardiac aging #MMPMID29967491 Lyu G; Guan Y; Zhang C; Zong L; Sun L; Huang X; Huang L; Zhang L; Tian XL; Zhou Z; Tao W Nat Commun 2018[]; 9 (ä): ä PMID29967491show ga Cellular senescence is a well-orchestrated programmed process involved in age-related pathologies, tumor suppression and embryonic development. TGF-?/Smad is one of the predominant pathways that regulate damage-induced and developmentally programmed senescence. Here we show that canonical TGF-? signaling promotes senescence via miR-29-induced loss of H4K20me3. Mechanistically, oxidative stress triggers TGF-? signaling. Activated TGF-? signaling gives rise to acute accumulation of miR-29a and miR-29c, both of which directly suppress their novel target, Suv4-20h, thus reducing H4K20me3 abundance in a Smad-dependent manner, which compromises DNA damage repair and genome maintenance. Loss of H4K20me3 mediated by the senescent TGF-?/miR-29 pathway contributes to cardiac aging in vivo. Disruption of TGF-? signaling restores H4K20me3 and improves cardiac function in aged mice. Our study highlights the sequential mechanisms underlying the regulation of senescence, from senescence-inducing triggers to activation of responsive signaling followed by specific epigenetic alterations, shedding light on potential therapeutic interventions in cardiac aging. äTGF-? signaling alters H4K20me3 status via miR-29 and contributes to c(epmc).pdf DeepDyve Pubget Overpricing