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High hydrostatic pressure participates in atrial fibrosis through the p300/p53/Smad3 pathway
The FASEB Journal ( IF 4.4 ) Pub Date : 2023-11-29 , DOI: 10.1096/fj.202300473rr
Shenghuan Yu 1 , Long Zeng 1 , Fang Rao 1, 2 , Chunyu Deng 1, 2 , Mengzhen Zhang 2 , Haiyin Xiao 2 , Feifei Xiao 1 , Yumei Xue 1, 3 , Shulin Wu 1, 3 , Zhimin Du 4 , Wei Wei 3
The FASEB Journal ( IF 4.4 ) Pub Date : 2023-11-29 , DOI: 10.1096/fj.202300473rr
Shenghuan Yu 1 , Long Zeng 1 , Fang Rao 1, 2 , Chunyu Deng 1, 2 , Mengzhen Zhang 2 , Haiyin Xiao 2 , Feifei Xiao 1 , Yumei Xue 1, 3 , Shulin Wu 1, 3 , Zhimin Du 4 , Wei Wei 3
Affiliation
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As an independent risk factor of atrial fibrillation (AF), hypertension (HTN) can induce atrial fibrosis through cyclic stretch and hydrostatic pressure. The mechanism by which high hydrostatic pressure promotes atrial fibrosis is unclear yet. p300 and p53/Smad3 play important roles in the process of atrial fibrosis. This study investigated whether high hydrostatic pressure promotes atrial fibrosis by activating the p300/p53/Smad3 pathway. Biochemical experiments were used to study the expression of p300/p53/Smad3 pathway in left atrial appendage (LAA) tissues of patients with sinus rhythm (SR), AF, AF + HTN, and C57/BL6 mice, hypertensive C57/BL6 mice and atrial fibroblasts of mice. To investigate the roles of p300 and p53 in the process of atrial fibrosis, p300 and p53 in mice atrial fibroblasts were knocked in or knocked down, respectively. The expression of p300/p53/Smad3 and fibrotic factors was higher in patients with AF and AF + HTN than those with SR only. The expressions of p300/p53/Smad3 and fibrotic factors increased in hypertensive mice. Curcumin (Cur) and knocking down of p300 reversed the expressions of these factors. 40 mmHg hydrostatic pressure/overexpression of p300 upregulated the expressions of p300/p53/Smad3 and fibrotic factors in mice LAA fibroblasts. While Cur or knocking down p300 reversed these changes. Knocking down/overexpression of p53, the expressions of p53/Smad3 and fibrotic factors also decreased/increased, correspondingly. High hydrostatic pressure promotes atrial fibrosis by activating the p300/p53/Smad3 pathway, which further increases the susceptibility to AF.
中文翻译：
高静水压通过p300/p53/Smad3通路参与心房纤维化
作为心房颤动（AF）的独立危险因素，高血压（HTN）可通过循环牵张和静水压诱发心房纤维化。高静水压促进心房纤维化的机制尚不清楚。 p300和p53/Smad3在心房纤维化过程中发挥重要作用。本研究探讨高静水压是否通过激活 p300/p53/Smad3 通路促进心房纤维化。采用生化实验研究窦性心律(SR)、AF、AF+HTN、C57/BL6小鼠、高血压C57/BL6小鼠和小鼠心房成纤维细胞。为了研究p300和p53在心房纤维化过程中的作用，分别敲入或敲低小鼠心房成纤维细胞中的p300和p53。 AF 和 AF + HTN 患者中 p300/p53/Smad3 和纤维化因子的表达高于仅 SR 患者。高血压小鼠p300/p53/Smad3和纤维化因子的表达增加。姜黄素 (Cur) 和 p300 的敲低逆转了这些因子的表达。 40 mmHg 静水压/p300 过表达上调小鼠 LAA 成纤维细胞中 p300/p53/Smad3 和纤维化因子的表达。而 Cur 或敲低 p300 则逆转了这些变化。敲低/过表达p53，p53/Smad3和纤维化因子的表达也相应减少/增加。高静水压通过激活p300/p53/Smad3通路促进心房纤维化，从而进一步增加房颤的易感性。
更新日期：2023-11-29
中文翻译：
高静水压通过p300/p53/Smad3通路参与心房纤维化
作为心房颤动（AF）的独立危险因素，高血压（HTN）可通过循环牵张和静水压诱发心房纤维化。高静水压促进心房纤维化的机制尚不清楚。 p300和p53/Smad3在心房纤维化过程中发挥重要作用。本研究探讨高静水压是否通过激活 p300/p53/Smad3 通路促进心房纤维化。采用生化实验研究窦性心律(SR)、AF、AF+HTN、C57/BL6小鼠、高血压C57/BL6小鼠和小鼠心房成纤维细胞。为了研究p300和p53在心房纤维化过程中的作用，分别敲入或敲低小鼠心房成纤维细胞中的p300和p53。 AF 和 AF + HTN 患者中 p300/p53/Smad3 和纤维化因子的表达高于仅 SR 患者。高血压小鼠p300/p53/Smad3和纤维化因子的表达增加。姜黄素 (Cur) 和 p300 的敲低逆转了这些因子的表达。 40 mmHg 静水压/p300 过表达上调小鼠 LAA 成纤维细胞中 p300/p53/Smad3 和纤维化因子的表达。而 Cur 或敲低 p300 则逆转了这些变化。敲低/过表达p53，p53/Smad3和纤维化因子的表达也相应减少/增加。高静水压通过激活p300/p53/Smad3通路促进心房纤维化，从而进一步增加房颤的易感性。
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