Article
Pharmacology & Pharmacy
Prachi Umbarkar, Anand P. Singh, Sultan Tousif, Qinkun Zhang, Palaniappan Sethu, Hind Lal
Summary: Nintedanib (NTB) is an FDA-approved tyrosine kinase inhibitor for pulmonary fibrosis, and study shows its potential in reducing cardiac fibrosis and improving cardiac function in a murine heart failure model, suggesting its promising application in treating HF patients.
PHARMACOLOGICAL RESEARCH
(2021)
Review
Biochemistry & Molecular Biology
Xiaonan Sun, Jalen Alford, Hongyu Qiu
Summary: Mitochondrial remodeling is crucial for maintaining normal cellular function and dysregulation can lead to complex diseases. Understanding the molecular basis and regulatory network of mitochondrial remodeling is important for elucidating the pathogenesis of cardiac diseases.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Health Care Sciences & Services
Barbara Ponikowska, Gracjan Iwanek, Agata Zdanowicz, Szymon Urban, Robert Zymlinski, Piotr Ponikowski, Jan Biegus
Summary: Heart failure is a major public concern with high incidence and prevalence, and the utility of various cardiovascular biomarkers in diagnosis and treatment is of significant importance, requiring further research.
JOURNAL OF PERSONALIZED MEDICINE
(2022)
Review
Biochemistry & Molecular Biology
Danilo Martins, Leonardo Rufino Garcia, Diego Aparecido Rios Queiroz, Taline Lazzarin, Carolina Rodrigues Tonon, Paola da Silva Balin, Bertha Furlan Polegato, Sergio Alberto Rupp de Paiva, Paula Schmidt Azevedo, Marcos Ferreira Minicucci, Leonardo Zornoff
Summary: Cardiac remodeling refers to a series of molecular, cellular, and interstitial changes in the heart that occur after different stimuli, manifesting clinically as changes in size, mass, geometry, and function. Remodeling plays a crucial pathophysiological role in the onset and progression of ventricular dysfunction. The role of oxidative stress as a therapeutic target for cardiac remodeling has been gaining attention in recent years.
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
Cardiac & Cardiovascular Systems
Hongmei Zhao, Hongqin Yang, Chi Geng, Yang Chen, Junling Pang, Ting Shu, Meijun Zhao, Yaqin Tang, Zhiwei Li, Baicun Li, Cuiliu Hou, Xiaomin Song, Aoxue Wu, Xiaoxiao Guo, Si Chen, Bin Liu, Chen Yan, Jing Wang
Summary: The study found that IgE plays a causative role in pathological cardiac remodeling, at least partially through activating IgE-Fc epsilon R1 signaling in cardiomyocytes and cardiac fibroblasts. Therapeutic strategies targeting the IgE-Fc epsilon R1 axis may be effective for managing IgE-mediated cardiac remodeling.
Article
Cardiac & Cardiovascular Systems
Gizem Keceli, Ashish Gupta, Joevin Sourdon, Refaat Gabr, Michael Schaer, Swati Dey, Carlo G. Tocchetti, Annina Stuber, Jacopo Agrimi, Yi Zhang, Michelle Leppo, Charles Steenbergen, Shenghan Lai, Lisa R. Yanek, Brian O'Rourke, Gary Gerstenblith, Paul A. Bottomley, Yibin Wang, Nazareno Paolocci, Robert G. Weiss
Summary: Abnormal energy metabolism in the heart is closely related to pathological remodeling in heart failure. Mitochondrial creatine kinase plays a critical role in attenuating maladaptive hypertrophy in heart failure by reducing reactive oxygen species levels and upregulating antioxidants.
CIRCULATION RESEARCH
(2022)
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
Cardiac & Cardiovascular Systems
Jin Li, Ane M. Salvador, Guoping Li, Nedyalka Valkov, Olivia Ziegler, Ashish Yeri, Chun Yang Xiao, Bessie Meechoovet, Eric Alsop, Rodosthenis S. Rodosthenous, Piyusha Kundu, Tianxiao Huan, Daniel Levy, John Tigges, Alexander R. Pico, Ionita Ghiran, Michael G. Silverman, Xiangmin Meng, Robert Kitchen, Jiahong Xu, Kendall Van Keuren-Jensen, Ravi Shah, Junjie Xiao, Saumya Das
Summary: miR-30d can improve cardiac function and reduce fibrosis by targeting MAP4K4 and integrin alpha 5, showing a protective effect in ischemic heart failure. The communication of extracellular vesicle-contained miRNAs may provide a novel therapeutic target in heart failure treatment.
CIRCULATION RESEARCH
(2021)
Article
Cardiac & Cardiovascular Systems
William W. Du, Jindong Xu, Weining Yang, Nan Wu, Feiya Li, Le Zhou, Sheng Wang, Xiangmin Li, Alina T. He, Kevin Y. Du, Kaixuan Zeng, Jian Ma, Juanjuan Lyu, Chao Zhang, Chi Zhou, Katarina Maksimovic, Burton B. Yang
Summary: The upregulation of circNlgn in patients with cardiac disease leads to cardiac overload. The novel peptide Nlgn173 binds to nuclear structural proteins and regulators, ultimately contributing to cardiac fibrosis and heart disease. Therapeutic implications may be derived from understanding this dysregulation mechanism.
CIRCULATION RESEARCH
(2021)
Article
Medicine, Research & Experimental
Mathieu Cinato, Laurie Guitou, Amira Saidi, Andrei Timotin, Erwan Sperazza, Thibaut Duparc, Sergey N. Zolov, Sai Srinivas Panapakkam Giridharan, Lois S. Weisman, Laurent O. Martinez, Jerome Roncalli, Oksana Kunduzova, Helene Tronchere, Frederic Boal
Summary: The study highlights the inhibitory effects of Apilimod on cardiac fibrotic remodeling, controlling the TGF beta signaling pathway to prevent adverse remodeling. It also suggests a novel function for PIKfyve in regulating myocardial fibrosis and TGF beta pathway.
Review
Biochemistry & Molecular Biology
Taline Lazzarin, Leonardo Rufino Garcia, Danilo Martins, Diego Aparecido Rios Queiroz, Carolina Rodrigues Tonon, Paola da Silva Balin, Bertha Furlan Polegato, Sergio Alberto Rupp de Paiva, Paula Schmidt Azevedo, Marcos Minicucci, Leonardo Zornoff
Summary: This review evaluates the role of nutrients and food as modulators of cardiac remodeling. Remodeling is associated with increased risk of heart disease, and antioxidative dietary compounds potentially have protective properties.
Article
Cardiac & Cardiovascular Systems
Javier Barallobre-Barreiro, Tamas Radovits, Marika Fava, Ursula Mayr, Wen-Yu Lin, Elizaveta Ermolaeva, Diego Martinez-Lopez, Eric L. Lindberg, Elisa Duregotti, Laszlo Daroczi, Maria Hasman, Lukas E. Schmidt, Bhawana Singh, Ruifang Lu, Ferheen Baig, Aleksandra Malgorzata Siedlar, Friederike Cuello, Norman Catibog, Konstantinos Theofilatos, Ajay M. Shah, Maria G. Crespo-Leiro, Nieves Domenech, Norbert Hubner, Bela Merkely, Manuel Mayr
Summary: The study identified ADAMTS5 protease as critical for versican degradation in the heart and found that versican accumulation is associated with impaired cardiac function in heart failure patients and animal models. Versikine, an ADAMTS-specific cleavage product, accumulated in ischemic heart failure patients and following cardiac ischemia/reperfusion injury in animal models. The use of beta-blockers in heart failure patients was associated with a reduction in ECM deposition, particularly in the levels of versican, indicating a potential beneficial effect on cardiac chondroitin sulfate proteoglycan content.
Review
Biochemistry & Molecular Biology
Lindsay Kraus, Brianna Beavens
Summary: Cardiovascular diseases are a leading global cause of death, lacking a cure. Epigenetics and chromatin remodeling have emerged as promising interventions. Recent advancements in bioinformatics and gene therapy have particularly advanced the field of chromatin remodeling, specifically for the treatment of heart failure. Understanding changes to chromatin architecture has revealed potential methods for altering the progression of cardiac diseases through genomic sequencing, targeting cardiac genes, utilizing RNA molecules, and employing chromatin remodeler complexes. This understanding may lead to individualized pharmaceutical interventions and biomarkers for major disease states, ultimately paving the way for future therapeutic approaches.
Article
Cardiac & Cardiovascular Systems
Lisa E. Dorn, William Lawrence, Jennifer M. Petrosino, Xianyao Xu, Thomas J. Hund, Bryan A. Whitson, Matthew S. Stratton, Paul M. L. Janssen, Peter J. Mohler, Anders Schlosser, Grith L. Sorensen, Federica Accornero
Summary: This study identified a novel role for nonmyocyte-derived MFAP4 in cardiac remodeling, playing a crucial role in cardiac adaptation to stress. Lack of MFAP4 resulted in increased cardiac hypertrophy, worsened cardiac function, and dysregulated G protein-coupled receptor and integrin signaling in the heart.
CIRCULATION RESEARCH
(2021)
