Article
Biochemistry & Molecular Biology
Jun Li, Ruoshui Li, Izabela Tuleta, Silvia C. Hernandez, Claudio Humeres, Anis Hanna, Bijun Chen, Nikolaos G. Frangogiannis
Summary: The role of macrophage Smad7 in regulating inflammation and repair after myocardial infarction is limited. The anti-inflammatory effects of TGF-beta in macrophages are not restrained by endogenous Smad7 induction.
Article
Pharmacology & Pharmacy
Meifang Wu, Yanguang Guo, Ying Wu, Kaizu Xu, Liming Lin
Summary: Sacubitril/valsartan has a significant improvement on cardiac function and fibrosis in rats after experimental myocardial infarction, by inhibiting collagen synthesis in myocardial fibroblasts through the suppression of the TGF/Smads signaling pathway.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Peripheral Vascular Disease
Yihai Liu, Chongxia Zhong, Jiayi Si, Shan Chen, Lina Kang, Biao Xu
Summary: This study found that Sacubitril/Valsartan can maintain cardiac function and reduce myocardial fibrosis in hypertensive patients early post myocardial infarction. This effect may occur prior to its antihypertensive effect.
JOURNAL OF HYPERTENSION
(2022)
Article
Plant Sciences
Bo Liang, Xiao-Xiao Zhang, Rui Li, Yong-Chun Zhu, Xiao-Jie Tian, Ning Gu
Summary: Guanxin V shows anti-oxidative, anti-apoptotic, and anti-fibrotic effects in acute myocardial infarction by alleviating oxidative stress damage and apoptosis induced by the TGF-beta 1 signaling pathway.
Article
Pharmacology & Pharmacy
Yong Fu, Jun Shi, Hong Qian, Chaoyi Qin, Lulu Liu, Jiayu Shen, Hao Ma, Lang Ma, Bin Liao, Yingqiang Guo
Summary: This study investigated the therapeutic effect of peritoneal matrix-loaded pirfenidone nanodroplets (NDs) on myocardial infarction (MI) fibrosis. The results showed that the nanodroplets achieved a slow drug release and inhibited cardiac fibroblasts transformation and collagen synthesis. Combining the peritoneal matrix with pirfenidone nanodroplets showed excellent therapeutic effects on fibrosis in MI rats. This study confirmed the feasibility and synergistic effectiveness of the approach and highlighted the potential application of nanomedicine in other biomedical fields.
EUROPEAN JOURNAL OF PHARMACOLOGY
(2022)
Article
Medicine, General & Internal
Xiaocheng Cheng, Liyou Wang, Xuesong Wen, Lei Gao, Guoxing Li, Guanglei Chang, Shu Qin, Dongying Zhang
Summary: The study investigated the role of TNAP in cardiac fibrosis after myocardial infarction, finding that high serum TNAP levels were associated with increased mortality in patients with ischemic heart disease and MI. The findings suggest that TNAP plays a crucial role in cardiac fibrosis by activating the TGF-beta/Smads and ERK1/2 signaling pathways.
Article
Plant Sciences
Ke-feng Zeng, Hui-juan Wang, Bo Deng, Ting-fang Chen, Jun-bang Chen, Wen-jun Ding, Si Chen, Jun-di Xie, Si-min Lu, Guang-hong Chen, Ying Zhang, Zhang-bin Tan, Hong-bin Ou, Yong-zhen Tan, Shuang-wei Zhang, Ying-chun Zhou, Jing-zhi Zhang, Bin Liu
Summary: This study found that ethyl ferulate (EF) attenuated myocardial fibrosis post-MI by directly suppressing TGFBR1 and its downstream signaling pathway.
Article
Medicine, Research & Experimental
Jingyao Yang, Long Li, Xiaoxiao Zheng, Zhaoyang Lu, Hua Zhou
Summary: As a sodium-glucose transporter 2 inhibitor (SGLT2i), Dapagliflozin (DAPA) has been widely recognized for its cardioprotective benefits. This study explored the underlying mechanisms of DAPA on angiotensin II (Ang II)-induced myocardial hypertrophy and found that DAPA treatment can alleviate Ang II-induced cardiac injury, hypertrophy, and fibrosis. It also reversed the changes in HIF-1a and SIRT1 levels induced by Ang II. Overall, activating the SIRT1/HIF-1a signaling pathway may be an effective therapeutic target for pathological cardiac hypertrophy.
BIOMEDICINE & PHARMACOTHERAPY
(2023)
Article
Pharmacology & Pharmacy
Rongheng Liao, Zhen Qi, Ri Tang, Renrong Wang, Yongyi Wang
Summary: The study revealed that MFA can alleviate fibrosis-related proteins expression, migration, and proliferation ability in human cardiac fibroblasts induced by TGF-beta 1, and improve fibrosis area, cardiac function, and fibrosis-related proteins expression in myocardial infarction mouse models. The mechanism involves MFA suppressing HCF differentiation by inhibiting migration and proliferation, through the pRB-E2F1/CCNE2 and the RhoA/ROCK2 pathway.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Plant Sciences
Junjun Li, Fuxing Ge, Shana Wuken, Shungang Jiao, Panlong Chen, Meiwen Huang, Xiaoli Gao, Juan Liu, Pengfei Tu, Xingyun Chai, Luqi Huang
Summary: This study aimed to investigate the cardioprotective properties and pharmacological mechanism of ZER against cardiac fibrosis. Animal experiments and in vitro studies showed that ZER can attenuate cardiac fibrosis and improve cardiac function by inhibiting the TGF-01/Smad signaling pathway.
Article
Biotechnology & Applied Microbiology
Youquan Chen, Ming Huang, Yi Yan, Dequan He
Summary: Tranilast exerts its ameliorative effect on myocardial fibrosis by inhibiting the S100A11/TGF-beta 1/Smad axis, thus providing a new research direction for the treatment of cardiac fibrosis.
Article
Oncology
Guiping Lu, Zhuowang Ge, Xinyuan Chen, Yue Ma, Ancai Yuan, Yuquan Xie, Jun Pu
Summary: In this study, it was found that BMP6 expression increased after myocardial infarction, and BMP6(-/-) mice showed more significant cardiac dysfunction and lower survival rates after MI. Additionally, BMP6(-/-) mice exhibited larger infarct area, increased fibrosis, and more pronounced inflammatory infiltration. Mechanistic studies revealed that BMP6 decreases collagen secretion in fibroblasts. Lastly, it was found that rhBMP6 can alleviate ventricular remodeling abnormalities after myocardial infarction.
CLINICAL AND TRANSLATIONAL MEDICINE
(2023)
Article
Biochemistry & Molecular Biology
Pema Raj, Karen Sayfee, Mihir Parikh, Liping Yu, Jeffrey Wigle, Thomas Netticadan, Shelley Zieroth
Summary: The study showed that in MI-induced rats, treatment with resveratrol, sacubitril/valsartan, and valsartan significantly prevented cardiac remodeling and dysfunction. These treatments worked by reducing cardiac oxidative stress, inflammation, and fibrosis, promoting heart health.
Article
Physiology
Mariela Beatriz Nolly, Lorena Alejandra Vargas, Maria Veronica Correa, Juan Manuel Lofeudo, Andres Oscar Pinilla, Jorge Omar Velez Rueda, Martin E. Guerrero-Gimenez, Erik Richard Swenson, Maria Teresa Damiani, Bernardo Victor Alvarez
Summary: The study found that after myocardial infarction, the interaction between CAIX and NBC1 to prevent acidic damage in hypoxic tissue may be a promising therapeutic target.
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
(2021)
Article
Cardiac & Cardiovascular Systems
Elias Daud, Offir Ertracht, Nadav Bandel, Gassan Moady, Monah Shehadeh, Tali Reuveni, Shaul Atar
Summary: Empagliflozin administered early post myocardial infarction reduces myocardial fibrosis and inhibits the TGF-beta 1/Smad3 fibrotic pathway, potentially before exerting any hemodynamic or physiological effects.
CARDIOVASCULAR DIABETOLOGY
(2021)