Article
Cardiac & Cardiovascular Systems
Ichitaro Abe, Takeshi Terabayashi, Katsuhiro Hanada, Hidekazu Kondo, Yasushi Teshima, Yumi Ishii, Miho Miyoshi, Shintaro Kira, Shotaro Saito, Hirotsugu Tsuchimochi, Mikiyasu Shirai, Kunio Yufu, Motoki Arakane, Tsutomu Daa, Dean Thumkeo, Shuh Narumiya, Naohiko Takahashi, Toshimasa Ishizaki
Summary: The study identified the pivotal role of mammalian homologue of Drosophila diaphanous (mDia) 1 in pressure overload-induced ventricular hypertrophy. Loss of mDia1 led to decreased cardiac hypertrophic responses and increased mortality rate in mice after aortic constriction, suggesting that mDia1 is crucial in compensatory cardiac hypertrophy in response to pressure overload.
CARDIOVASCULAR RESEARCH
(2021)
Article
Cardiac & Cardiovascular Systems
Patrick M. Pilz, Jennifer E. Ward, Wei-Ting Chang, Attila Kiss, Edward Bateh, Alokkumar Jha, Sudeshna Fisch, Bruno K. Podesser, Ronglih Liao
Summary: This article outlines the strengths, limitations, and outcomes of small and large animal models of heart failure with reduced ejection fraction currently used in basic and translational research. Animal models play a critical role in understanding the molecular mechanisms of heart failure, although no model completely recapitulates the full human disease.
CIRCULATION RESEARCH
(2022)
Article
Biochemical Research Methods
Mona Malek Mohammadi, Aya Abouissa, Joerg Heineke
Summary: A neonatal mouse model of pressure overload by transverse aortic constriction (nTAC) was established, demonstrating different responses in mice at different postnatal stages, which could facilitate future research on therapeutic strategies.
Article
Chemistry, Multidisciplinary
Ajit Magadum, Neha Singh, Ann Anu Kurian, Mohammad Tofael Kabir Sharkar, Nishat Sultana, Elena Chepurko, Keerat Kaur, Magdalena M. Zak, Yoav Hadas, Djamel Lebeche, Susmita Sahoo, Roger Hajjar, Lior Zangi
Summary: Heart failure remains a major issue globally, with cardiac hypertrophy and fibrosis being key factors. The regulator Pip4k2c, associated with mTORC1, plays a role in these processes. Studies show that deleting Pip4k2c does not affect embryonic cardiac development, but leads to increased rates of CH, CF, and sudden death in adult mice. Upregulating Pip4k2c improves heart function, reverses CH and CF, and enhances survival through inhibiting TGF beta 1 via specific pathways. Loss-and-gain-of-function studies identify Pip4k2c as a potential therapeutic target for CF, CH, and HF, utilizing modRNA as an effective gene therapy approach.
Article
Medicine, Research & Experimental
Yizhou Feng, Yuan Yuan, Hongxia Xia, Zhaopeng Wang, Yan Che, Zhefu Hu, Jiangyang Deng, Fangfang Li, Qingqing Wu, Zhouyan Bian, Heng Zhou, Difei Shen, Qizhu Tang
Summary: OSMR deficiency exacerbates pressure overload-induced cardiac hypertrophy by modulating macrophages and OSM/LIFR/STAT3 signaling, suggesting that OSMR may be a potential target for treating pathological cardiac hypertrophy and heart failure.
JOURNAL OF TRANSLATIONAL MEDICINE
(2023)
Article
Cardiac & Cardiovascular Systems
Jin-Ling Huo, Lemin Jiao, Qi An, Xiuying Chen, Yuruo Qi, Bingfei Wei, Yichao Zheng, Xiaojing Shi, Erhe Gao, Hong-Min Liu, Dong Chen, Cong Wang, Wen Zhao
Summary: This study evaluates the roles of myofibroblast- or cardiomyocyte-specific LSD1 deficiency in pressure overload-induced cardiac remodeling. The findings suggest that myofibroblast-specific LSD1 deletion attenuates transverse aortic constriction-induced cardiac remodeling and improves heart function, highlighting LSD1 as a potential therapeutic target for late-stage heart failure.
CIRCULATION RESEARCH
(2021)
Article
Cardiac & Cardiovascular Systems
Xavier Revelo, Preethy Parthiban, Chen Chen, Fanta Barrow, Gavin Fredrickson, Haiguang Wang, Dogacan Yucel, Adam Herman, Jop H. van Berlo
Summary: This study assessed the role of cardiac immune cells in the early hypertrophy response to cardiac pressure overload and found that cardiac resident macrophages play a key role in stimulating angiogenesis and inhibiting fibrosis in response to cardiac pressure overload.
CIRCULATION RESEARCH
(2021)
Article
Cardiac & Cardiovascular Systems
Jinxi Wang, Qian Shi, Yihui Wang, Logan W. Dawson, Grace Ciampa, Weiyang Zhao, Guangqin Zhang, Biyi Chen, Robert M. Weiss, Chad E. Grueter, Duane D. Hall, Long-Sheng Song
Summary: This study demonstrates the potential of JP2NT gene therapy in attenuating transcriptional remodeling and development of heart failure induced by cardiac stress. The findings suggest that JP2NT gene therapy may serve as a novel therapeutic approach for treating hypertrophy and heart failure.
CIRCULATION RESEARCH
(2022)
Review
Biochemistry & Molecular Biology
David Aluja, Sara Delgado-Tomas, Marisol Ruiz-Meana, Jose A. Barrabes, Javier Inserte
Summary: Despite advances in treatment, heart failure remains a major cause of illness and death. Preventing myocardial hypertrophy, which is an independent risk factor for heart failure, is a clinical objective. Recent studies suggest that calpains, a type of protein, play a role in the development of cardiac hypertrophy, and inhibiting calpains may be a potential pharmacological strategy. New compounds are being developed and tested in animal models to evaluate the effectiveness of calpain inhibition in treating pathological cardiac hypertrophy.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Cardiac & Cardiovascular Systems
Lin Yuan, Shichen Bu, Meng Du, Yilong Wang, Chenhui Ju, Dandan Huang, Wenjing Xu, Xin Tan, Minglu Liang, Shan Deng, Liu Yang, Kai Huang
Summary: This study investigated the role of RNF207 in the development of pathological cardiac hypertrophy and dysfunction. The results showed that RNF207 exacerbated cardiac hypertrophy and fibrosis, while RNF207 knockdown alleviated these conditions.
CARDIOVASCULAR RESEARCH
(2023)
Article
Cardiac & Cardiovascular Systems
Pei -Wen Liu, Gregory L. Martin, Weiyu Lin, Wanting Huang, Suchita Pande, Mark J. Aronovitz, Roger J. Davis, Robert M. Blanton
Summary: This study identified the role of the MLK3 CRIB domain in regulating basal blood pressure and cardiac morphology, as well as promoting the compensatory left ventricular response to pressure overload.
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Hairuo Lin, Yingqi Zhu, Cankun Zheng, Donghong Hu, Siyuan Ma, Lin Chen, Qiancheng Wang, Zhenhuan Chen, Jiahe Xie, Yi Yan, Xiaobo Huang, Wangjun Liao, Masafumi Kitakaze, Jianping Bin, Yulin Liao
Summary: Exercise-induced myocardial hypertrophy preconditioning can increase myocardial resistance to pathological stress through an antihypertrophic effect mediated by the Mhrt779/Brg1/Hdac2/p-Akt/p-GSK3 beta signaling pathway.
Article
Biochemistry & Molecular Biology
Manabu Shiraishi, Ken Suzuki, Atsushi Yamaguchi
Summary: Excess deposition of extracellular matrix in the myocardium is associated with reduced left ventricular function. The mechanisms underlying the reversal of fibrosis are not well understood. This study investigated the role of myocardial tissue elasticity in influencing fibroblast phenotype. In vitro experiments using different culture conditions showed that fibroblasts differentiated into activated or matrix-degrading types based on the pericellular environment. Gene expression analysis identified Selenbp1 as a key regulator of fibroblast differentiation. Knockdown of Selenbp1 enhanced fibroblast activation and inhibited matrix degradation. In vivo knockdown of Selenbp1 resulted in tissue fibrosis and diastolic failure in the left ventricle. Selenbp1 appears to be a major molecule involved in regulating collagen turnover in cardiac fibrosis.
Article
Cardiac & Cardiovascular Systems
Daniel Burkhoff, Veli K. Topkara, Gabriel Sayer, Nir Uriel
Summary: This review provides a comprehensive overview of research into LVAD therapy for heart failure, including the hemodynamic effects of LVAD support and the structural, cellular, and molecular aspects of LVAD-associated reverse remodeling. The review also discusses the synergistic effects of LVAD support with heart failure therapies on clinical outcomes and myocardial biology.
CIRCULATION RESEARCH
(2021)
Article
Cell Biology
Peilei Lu, Fan Ding, Yang Kevin Xiang, Liying Hao, Meimi Zhao
Summary: This article discusses the roles of various ncRNAs, including miRNAs, lncRNAs, and circRNAs, in modulating cardiac hypertrophy and heart failure in cardiovascular diseases.