Article
Medicine, Research & Experimental
Pascal Syren, Ann-Kathrin Rahm, Patrick A. Schweizer, Claus Bruehl, Hugo A. Katus, Norbert Frey, Dierk Thomas, Patrick Lugenbiel
Summary: The study suggests that the suppression of histone deacetylase 2 (HDAC2) is associated with ventricular electrical remodeling, ion channel expression, and the pathophysiological process of early heart failure.
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
Jun Luo, Stephen D. D. Farris, Deri Helterline, April Stempien-Otero
Summary: Cardiomyocytes increase DNA content in response to stress in humans, but this study found that DNA content decreases in unloaded hearts. Changes in DNA content were independent of cell proliferation. The study used a novel imaging flow cytometry methodology to compare human subjects with LVAD implantation or primary transplantation. Results showed that cardiomyocyte size decreased and DNA content per nucleus significantly decreased in unloaded hearts, while cell-cycle markers were not increased.
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Masafumi Funamoto, Yoichi Sunagawa, Yasufumi Katanasaka, Kana Shimizu, Yusuke Miyazaki, Nurmila Sari, Satoshi Shimizu, Kiyoshi Mori, Hiromichi Wada, Koji Hasegawa, Tatsuya Morimoto
Summary: This study reveals the importance of stage-specific histone acetylation in the development and progression of heart failure, providing new insights into the transcriptional regulatory mechanisms governing hypertrophic response genes.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Biology
Robert A. Eder, Maaike van den Boomen, Salva R. Yurista, Yaiel G. Rodriguez-Aviles, Mohammad Rashedul Islam, Yin-Ching Iris Chen, Lena Trager, Jaume Coll-Font, Leo Cheng, Haobo Li, Anthony Rosenzweig, Christiane D. Wrann, Christopher T. Nguyen
Summary: This study reveals that exercise training induces regional remodeling of the heart's microstructural tissue, and the expression of the CITED4 gene is necessary for this process.
COMMUNICATIONS BIOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Joanne F. Garbincius, Timothy S. Luongo, Pooja Jadiya, Alycia N. Hildebrand, Devin W. Kolmetzky, Adam S. Mangold, Rajika Roy, Jessica Ibetti, Mary Nwokedi, Walter J. Koch, John W. Elrod
Summary: The study demonstrates the importance of mitochondrial calcium in early pathological remodeling in non-ischemic heart disease, but also highlights a deleterious consequence of increasing mCa(2+) efflux when the heart is subjected to extreme, sustained neurohormonal stress.
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
(2022)
Article
Physiology
Yaofang Zhang, Lingyu Ye, Dayue Darrel Duan, Hong Yang, Tonghui Ma
Summary: This study investigates the role of TMEM16A in cardiac remodeling and angiogenesis. The results show that TMEM16A has insignificant contribution to myocardium remodeling during pressure overload. However, TMEM16A is a positive regulator of migration and angiogenesis under normal conditions or simulated stress. TMEM16A may become a new target for upregulation of angiogenesis in ischemic disorders like ischemic heart disease.
FRONTIERS IN PHYSIOLOGY
(2022)
Review
Pharmacology & Pharmacy
Hae Jin Kee, Inkyeom Kim, Myung Ho Jeong
Summary: This article provides an overview of the pathogenesis of hypertension, current anti-hypertensive drugs, and the need for novel drugs. It focuses on the role and regulatory mechanisms of HDACs in hypertension and discusses the progress in developing HDAC inhibitors as potential therapeutic targets.
BIOCHEMICAL PHARMACOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Alan J. Mouton, Elizabeth R. Flynn, Sydney P. Moak, Xuan Li, Alexandre A. da Silva, Zhen Wang, Jussara M. do Carmo, Michael E. Hall, John E. Hall
Summary: Obesity alone does not cause cardiac injury or exacerbate hypertension-induced cardiac dysfunction. After MI, obese-normotensive mice had lower survival rates compared with chow-fed mice, and this was further decreased by hypertension. Surviving obese-normotensive mice displayed improved post-MI cardiac function and metabolism, while these favorable changes were attenuated by hypertension when it accompanied obesity.
JOURNAL OF THE AMERICAN HEART ASSOCIATION
(2021)
Article
Cardiac & Cardiovascular Systems
Vivien Ngo, Bernd K. Fleischmann, Manfred Jung, Lutz Hein, Achim Lother
Summary: This study evaluated the potential of 4 epigenetic drugs to prevent adverse gene expression in cardiac myocytes. The HDAC6 inhibitor JS28 was found to be the most effective in preventing pathological gene expression with minimal impact on physiological gene expression. Genome-wide chromatin binding profiles revealed distinct effects of HDAC6 and BRD4 inhibitors on gene expression.
JOURNAL OF THE AMERICAN HEART ASSOCIATION
(2022)
Article
Chemistry, Multidisciplinary
Fang-fang Ren, Lin Zhao, Xian-yun Jiang, Jing-jing Zhang, Jia-min Gou, Xiao-yu Yu, Shu-jin Wu, Lei Li
Summary: Apoptosis, or programmed cell death, plays a critical role in the development of heart failure. Sphingosylphosphorylcholine (SPC), a bioactive sphingolipid, has been shown to inhibit apoptosis in myofibroblasts, non-muscle cells in the heart. In this study, the researchers investigated the role of the SPC receptor, calmodulin (CaM), in cardiomyocyte apoptosis and the associated signaling pathways. They found that SPC administration improved survival rate, cardiac hypertrophy, and cardiac fibrosis in mice with pressure overload-induced heart failure. In cardiomyocytes, SPC treatment inhibited cardiomyocyte hypertrophy, fibroblast-to-myofibroblast transition, and cell apoptosis. This was accompanied by reduced levels of pro-apoptotic proteins and phosphorylation of CaM, JNK, and p38, as well as increased levels of a cardiomyocyte-protective protein. The protective effect of SPC was annulled by a compound that increased CaM function. The researchers also demonstrated that SPC-mediated inhibition of cardiomyocyte apoptosis involved the regulation of p38 and JNK phosphorylation, which was downstream of CaM. These findings provide new evidence for SPC regulation of cardiomyocyte apoptosis and suggest it as a potential therapeutic target for cardiac remodeling following stress overload.
ACTA PHARMACOLOGICA SINICA
(2023)
Article
Cardiac & Cardiovascular Systems
Gun Jik Kim, Hanna Jung, Eunjo Lee, Sung Woon Chung
Summary: Histone deacetylase (HDAC) inhibitors, such as mocetinostat, have been shown to regulate cardiac remodeling and reduce fibrosis in rat models with TAC-induced pressure overload cardiac hypertrophy. This study indicates that mocetinostat has cardiorenal protective effects by decreasing cardiac and renal fibrosis and reducing activity of RAS-related components. Therefore, mocetinostat may be a promising therapeutic agent for hypertension-related diseases.
REVIEWS IN CARDIOVASCULAR MEDICINE
(2021)
Review
Cardiac & Cardiovascular Systems
Jian Qin, Ningning Guo, Jingjing Tong, Zhihua Wang
Summary: Cardiac hypertrophy is a common pathological process in cardiovascular diseases, characterized by gene expression reprogramming largely dependent on histone modifications such as methylation and acetylation. Understanding the role of histone modifiers in cardiac hypertrophy provides potential therapeutic strategies.
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
(2021)
Article
Cardiac & Cardiovascular Systems
Jessica Gambardella, Stanislovas S. Jankauskas, Urna Kansakar, Fahimeh Varzideh, Roberta Avvisato, Nella Prevete, Simone Sidoli, Pasquale Mone, Xujun Wang, Angela Lombardi, Gaetano Santulli
Summary: This study conducted comprehensive in vivo and in vitro experiments to investigate the molecular processes underlying ischemic cardiac disease. The findings revealed a specific pattern of chromatin remodeling induced by ischemic injury, which led to the transcriptional repression of a key regulator of mitochondrial function. Additionally, the study discovered a novel pathway linking metabolism to gene expression, demonstrating the role of ketone bodies in modulating chromatin remodeling and mitochondrial dysfunction.
JACC-BASIC TO TRANSLATIONAL SCIENCE
(2023)
Article
Multidisciplinary Sciences
Stefanie Maria Werhahn, Julia S. Kreusser, Marco Hagenmuller, Jan Beckendorf, Nathalie Diemert, Sophia Hoffmann, Jobst-Hendrik Schultz, Johannes Backs, Matthias Dewenter
Summary: Chronic isoproterenol (ISO) infusion induces both maladaptive remodelling and adaptive PKA signalling to maintain cardiac function, highlighting the complex role of beta-adrenergic signaling in heart failure._Stoppage of ISO leads to progressive worsening of cardiac function, indicating the delicate balance between adaptive and maladaptive effects of beta-adrenergic stimulation.
