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)
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)
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
Scott A. Hinger, Jiangbo Wei, Lisa E. Dorn, Bryan A. Whitson, Paul M. L. Janssen, Chuan He, Federica Accornero
Summary: The study found an increased m(6)A content in human heart failure samples, with m(6)A-regulated sites enriched in targeted transcripts involved in histone modification in heart failure patients. Additionally, shared transcripts targeted by m(6)A under stress conditions and unique m(6)A events in unstressed cardiomyocytes were identified, indicating the potential impact of m(6)A on post-transcriptional regulation of gene expression in the heart.
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
(2021)
Article
Pharmacology & Pharmacy
Ravi Sonkar, Ryan Berry, Mary N. Latimer, Sumanth D. Prabhu, Martin E. Young, Stuart J. Frank
Summary: Circadian clocks regulate various biological processes, including hormone secretion and target tissue sensitivity. This study found that genetic disruption of the cardiomyocyte circadian clock leads to cardiomyopathy, potentially due to excessive activation of cardiac GH/IGF1 signaling.
FRONTIERS IN 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
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)
Article
Cardiac & Cardiovascular Systems
Drew Theobald, Anand R. Nair, Srinivas Sriramula, Joseph Francis
Summary: Toll-like receptor 4 (TLR4) plays a crucial role in the innate immune response and cardiovascular diseases. This study found that cardiomyocyte-specific deletion of TLR4 provides protection against hypertension, cardiac hypertrophy, and remodeling. The results showed that in mice with cardiomyocyte-specific TLR4 knockdown, angiotensin II-induced hypertension and cardiac hypertrophy were attenuated, myocardial fibrosis was reduced, and cardiac function was improved.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2023)
Article
Cell Biology
Satoshi Kawaguchi, Bruno Moukette, Marisa N. Sepulveda, Taiki Hayasaka, Tatsuya Aonuma, Angela K. Haskell, Jessica Mah, Suthat Liangpunsakul, Yaoliang Tang, Simon J. Conway, Il-man Kim
Summary: miR-150 is downregulated during heart failure and correlates with patient outcomes. It protects against myocardial infarction by reducing cardiomyocyte apoptosis and targets small proline-rich protein 1a. Knockdown of SPrr1a improves cardiac dysfunction and fibrosis post-MI.
CELL DEATH & DISEASE
(2023)
Article
Multidisciplinary Sciences
Kirsten T. Nijholt, Pablo I. Sanchez-Aguilera, Harmen G. Booij, Silke U. Oberdorf-Maass, Martin M. Dokter, Anouk H. G. Wolters, Ben N. G. Giepmans, Wiek H. van Gilst, Joan H. Brown, Rudolf A. de Boer, Herman H. W. Sillje, B. Daan Westenbrink
Summary: This study aimed to determine if AKIP1 promotes physiological cardiomyocyte hypertrophy in vivo. The results showed that AKIP1-TG mice exhibited increased exercise-induced cardiac hypertrophy compared to wild type mice. AKIP1 may serve as a regulator of cardiomyocyte elongation and physiological cardiac remodelling.
SCIENTIFIC REPORTS
(2023)
Article
Biochemistry & Molecular Biology
Guojian Fang, Yingze Li, Jiali Yuan, Wei Cao, Shuai Song, Long Chen, Yuepeng Wang, Qunshan Wang
Summary: Heart failure is a severe and life-threatening disease worldwide. Cadherin-11 (Cad-11) is highly expressed in the heart and associated with inflammation. The study found that Cad-11 is increased in heart failure patients and plays a role in ventricular remodeling. Cad-11 deficiency improved pressure overload-induced structural and electrical remodeling in mice. Furthermore, Cad-11 induces IL-6 secretion from cardiac fibroblasts, which modulates the pathophysiology of neighboring cardiomyocytes.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Biochemistry & Molecular Biology
Mark Sweeney, Katie O'Fee, Chelsie Villanueva-Hayes, Ekhlas Rahman, Michael Lee, Konstantinos Vanezis, Ivan Andrew, Wei-Wen Lim, Anissa Widjaja, Paul J. R. Barton, Stuart A. Cook
Summary: This study demonstrates that IL11 expression in cardiomyocytes can lead to severe cardiac fibrosis and inflammation, as well as endothelial-to-mesenchymal transition and left ventricular dysfunction.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
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
Qing Liang, Hu Xu, Min Liu, Lei Qian, Jin Yan, Guangrui Yang, Lihong Chen
Summary: Cardiomyocyte-specific deletion of Bmal1 promotes pressure overload-induced cardiac remodeling, potentially through the activation of the PI3K/AKT signaling pathway.
JOURNAL OF THE AMERICAN HEART ASSOCIATION
(2022)
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
Kashvi Gupta, Ioannis Mastoris, Andrew J. Sauer
HEART FAILURE CLINICS
(2024)
Review
Cardiac & Cardiovascular Systems
Alexander L. Wallner, Salvatore Savona, Rami Kahwash
HEART FAILURE CLINICS
(2024)
Article
Cardiac & Cardiovascular Systems
Muhammad Shahzeb Khan, Anousheh Awais Paracha, Jan Biegus, Rafael de la Espriella, Julio Nunez, Carlos G. Santos-Gallego, Dmitry Yaranov, Marat Fudim
Summary: The increase of preload in heart failure can lead to excessive intracardiac pressures. The reduction of preload can be achieved through pharmacological and nonpharmacological interventions, with nonpharmacological interventions aiming to reduce blood inflow or increase splanchnic vascular blood pooling.
HEART FAILURE CLINICS
(2024)
Article
Cardiac & Cardiovascular Systems
Parin J. Patel, Asim S. Ahmed
HEART FAILURE CLINICS
(2024)
Article
Cardiac & Cardiovascular Systems
Husam M. Salah, Claudia Baratto, Dmitry M. Yaranov, Karl-Philipp Rommel, Satyanarayana Achanta, Sergio Caravita, Vinay Kumar Reddy Vasanthu, Marat Fudim
HEART FAILURE CLINICS
(2024)
Article
Cardiac & Cardiovascular Systems
Gregory R. Jackson, Abhinav Singh
HEART FAILURE CLINICS
(2024)
Review
Cardiac & Cardiovascular Systems
Ronald D. Bass, Joseph Phillips, Jorge Sanz Sanchez, Priti Shah, Stephen Sum, Ron Waksman, Hector M. Garcia-Garcia
Summary: NIRS-derived LCBI is an effective measurement for identifying vulnerable patients and plaques at risk of future adverse events. Patients with an elevated LCBI have higher odds of enduring a future adverse event.
HEART FAILURE CLINICS
(2024)
Article
Cardiac & Cardiovascular Systems
Adam Bland, Eunice Chuah, William Meere, Thomas J. Ford
Summary: CMD is a challenging condition to manage due to its heterogenous pathophysiology, presentation, and response to therapy. Although awareness of CMD is improving, there is a lack of randomized trials for therapy. Invasive assessment of the coronary microcirculation can improve patient-centered outcomes. Beta-blockers are the cornerstone of therapy for CMD angina, and non-pharmacological interventions play a central role in management. Further research is needed to assess the impact of traditional and novel pharmacological therapies on symptoms and clinical events in different CMD endotypes.
HEART FAILURE CLINICS
(2024)
