miR-214 could promote myocardial fibrosis and cardiac mesenchymal transition in VMC mice through regulation of the p53 or PTEN-PI3K-Akt signali pathway, promoting CF proliferation and inhibiting its ng pathway

Huang, Xianggui; Zheng, Danling; Liu, Chong; Huang, Jianxiang; Chen, Xiaoshan; Zhong, Jialin; Wang, Jing; Lin, Xinyue; Zhao, Chengkuan; Chen, Meini; Su, Siman; Chen, Yun; Xu, Chengcheng; Lin, Chaoxian; Huang, Yihui; Zhang, Shuyao

doi:10.1016/j.intimp.2023.110765

Cited by 1 publication

(1 citation statement)

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“…Myocardial fibrosis includes three categories: reactive myocardial fibrosis, replacement myocardial fibrosis, and infiltrative myocardial fibrosis. Reactive myocardial fibrosis is more common in hypertension [ 57 ], heart valve disease [ 58 , 59 ], viral myocarditis [ 59 , 60 ], and dilated cardiomyopathy [ 60 ]. The mechanism is increased pressure or volume load leading to an increase in collagen fibers surrounding the heart vessels but without myocardial cell loss or significant scarring [ 61 ].…”

Section: Discussionmentioning

confidence: 99%

Optimized New Shengmai Powder modulation of cAMP/Rap1A signaling pathway attenuates myocardial fibrosis in heart failure

Zhang,

xu,

Wang

et al. 2024

Chin Med

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Background Optimized New Shengmai Powder (ONSMP) is a traditional Chinese medicine formula with significant anti-heart failure and myocardial fibrosis effects, but the specific molecular biological mechanisms are not fully understood. Methods In this study, we first used network pharmacology to analyze the ONSMP's active ingredients, core signaling pathways, and core targets. Second, calculate the affinity and binding modes of the ONSMP components to the core targets using molecular docking. Finally, the heart failure rat model was established by ligating the left anterior descending branch of the coronary artery and assessing the effect of ONSMP on myocardial fibrosis in heart failure using echocardiography, cardiac organ coefficients, heart failure markers, and pathological sections after 4 weeks of drug intervention. The cAMP level in rat myocardium was determined using Elisa, the α-SMA and FSP-1 positive expression determined by immunohistochemistry, and the protein and mRNA levels of the cAMP/Rap1A signaling pathway were detected by Western Blotting and quantitative real-time PCR, respectively. Results The result shows that the possible mechanism of ONSMP in reducing myocardial fibrosis also includes the use of 12 active ingredients such as baicalin, vitamin D, resveratrol, tanshinone IIA, emodin, 15,16-dihydrotanshinone-i to regulate β1-AR, AC6, EPAC1, Rap1 A, STAT3, and CCND1 on the cAMP/Rap1A signaling pathway, thereby inhibiting the proliferation of cardiac fibroblasts and reduce the excessive secretion of collagen, effectively improve cardiac function and ventricular remodeling in heart failure rats. Conclusion This research shows that ONSMP can inhibit myocardial fibrosis and delay heart failure through the cAMP/Rap1A signaling pathway.

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