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
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
Medicine, Research & Experimental
Suman Dalal, Paige L. Shook, Mahipal Singh, Krishna Singh
Summary: This study investigates the cardioprotective effect of exogenous ubiquitin (UB) treatment in a mouse model of myocardial ischemia/reperfusion (I/R) injury. The results show that UB treatment improves heart function and reduces myocardial fibrosis, apoptosis, hypertrophy, and serum cytokine/chemokine levels.
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
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)
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
Hao-Ran Li, Xiao-Ming Zheng, Yan Liu, Jing-Hui Tian, Jie-Jian Kou, Jun-Zhuo Shi, Xiao-Bin Pang, Xin-Mei Xie, Yu Yan
Summary: This study demonstrates that L-carnitine (LC) has a cardioprotective effect in mice following myocardial infarction (MI), reducing cardiac fibrosis and improving cardiac function. LC treatment reduces inflammatory response and activation of the apoptotic signaling pathway.
CARDIOVASCULAR THERAPEUTICS
(2022)
Article
Biochemistry & Molecular Biology
Jung Joo Yoon, Chan Ok Son, Hye Yoom Kim, Byung Hyuk Han, Yun Jung Lee, Ho Sub Lee, Dae Gill Kang
Summary: The study showed that DOX induces cardiac hypertrophy in H9c2 cells, but BA treatment can suppress these pathological responses and inhibit ROS generation. In addition, BA also blocks the phosphorylation of JNK, ERK, and p38, and improves the GATA-4 and calcineurin/NFAT-3 signaling pathway activation induced by DOX in H9c2 cells. Furthermore, BA treatment reduces DOX-induced cell apoptosis and regulates the protein expression levels of Bcl-2, Bax, and cleaved caspase-3/-9.
Article
Medicine, General & Internal
Fatih Yalcin, Hulya Yalcin, Nagehan Kucukler, Serbay Arslan, Oguz Akkus, Alparslan Kurtul, Maria Roselle Abraham
Summary: This review article discusses the importance of hypertension in the development of left ventricular remodeling and heart failure, focusing on the early imaging biomarker of basal septal hypertrophy (BSH). The validation of BSH through animal studies and clinical observations is also addressed. Furthermore, the evaluation of quantitative imaging studies in both human and animal models, as well as the significance of combined cardiac imaging methods and stress-induction, are emphasized in separating adaptive and maladaptive phases of left ventricular remodeling.
JOURNAL OF CLINICAL MEDICINE
(2022)
Article
Cardiac & Cardiovascular Systems
Tomoki Sakata, Renata Mazurek, Spyros A. Mavropoulos, Francisco J. Romeo, Anjali J. Ravichandran, Shin Watanabe, Taro Kariya, Kiyotake Ishikawa
Summary: The etiology of mitral regurgitation (MR) affects left atrial (LA) remodeling and function differently. Severe ischemic MR leads to extensive LA remodeling and reduced function, which may contribute to poor clinical outcomes. Detailed assessment of LA remodeling is important for managing ischemic MR.
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Mareomi Hamada, Akiyoshi Ogimoto, Takashi Otani, Kiyotaka Ohshima, Tamami Kono, Yuta Watanabe, Tatsuro Tasaka, Shuntaro Ikeda
Summary: The study found that the progression of LVH in hypertension did not lead to abnormal LV systolic function, but afterload mismatch was observed in patients with LVHF. Exhaustion of preload reserve led to afterload mismatch in group III.
INTERNATIONAL JOURNAL OF CARDIOLOGY
(2022)
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
Menglong Wang, Mengmeng Zhao, Junping Yu, Yao Xu, Jishou Zhang, Jianfang Liu, Zihui Zheng, Jing Ye, Zhen Wang, Di Ye, Yongqi Feng, Shuwan Xu, Wei Pan, Cheng Wei, Jun Wan
Summary: This study investigated the effects of the selective NLRP3 inhibitor MCC950 on heart failure (HF) induced by pressure overload in obese mice and its metabolic mechanism. The results showed that MCC950 improved cardiac hypertrophy, fibrosis, and inflammation in obese mice. It also promoted M2 macrophage infiltration and regulated fatty acid and glucose uptake and utilization. Additionally, MCC950 affected the phosphorylation of AKT and AMPK in obese mice with HF.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2022)
Article
Multidisciplinary Sciences
Bianca de Moraes Fracasso, Juliana Oliveira Rangel, Alessandra Goncalves Machado, Fernanda Severo Curuja, Amanda Lopes, Virgilio Olsen, Nadine Clausell, Andreia Biolo, Luis Eduardo Rohde, Michael Andrades
Article
Biochemistry & Molecular Biology
Denis A. Mogilenko, Joel T. Haas, Laurent L'homme, Sebastien Fleury, Sandrine Quemener, Matthieu Levavasseur, Coralie Becquart, Julien Wartelle, Alexandra Bogomolova, Laurent Pineau, Olivier Molendi-Coste, Steve Lancel, Helene Dehondt, Celine Gheeraert, Aurelie Melchior, Cedric Dewas, Artemii Nikitin, Samuel Pic, Nabil Rabhi, Jean-Sebastien Annicotte, Seiichi Oyadomari, Talia Velasco-Hernandez, Jorg Cammenga, Marc Foretz, Benoit Viollet, Milica Vukovic, Arnaud Villacreces, Kamil Kranc, Peter Carmeliet, Guillemette Marot, Alexis Boulter, Simon Tavernier, Luciana Berod, Maria P. Longhi, Christophe Paget, Sophie Janssens, Delphine Staumont-Salle, Ezra Aksoy, Bart Staels, David Dombrowicz
Article
Genetics & Heredity
Mariana Recamonde-Mendoza, Adriano V. Werhli, Andreia Biolo
Article
Cardiac & Cardiovascular Systems
Luis E. Rohde, Marciane M. Rover, Jose A. Figueiredo Neto, Luiz C. Danzmann, Eduardo G. Bertoldi, Marcus Simoes, Odilson M. Silvestre, Antonio L. P. Ribeiro, Lidia Zytynski Moura, Luis Beck-da-Silva, Debora Prado, Roberto T. Sant'Anna, Leonardo H. Bridi, Andre Zimerman, Priscila Raupp da Rosa, Andreia Biolo
EUROPEAN HEART JOURNAL
(2019)
Article
Endocrinology & Metabolism
Camille Marciniak, Christian Duhem, Alexis Boulinguiez, Violeta Raverdy, Gregory Baud, Helene Verkindt, Robert Caiazzo, Bart Staels, Helene Duez, Francois Pattou, Steve Lancel
ACTA DIABETOLOGICA
(2020)
Article
Multidisciplinary Sciences
Sarah Ducastel, Veronique Touche, Mohamed-Sami Trabelsi, Alexis Boulinguiez, Laura Butruille, Margaux Nawrot, Simon Peschard, Oscar Chavez-Talavera, Emilie Dorchies, Emmanuelle Vallez, Jean-Sebastien Annicotte, Steve Lancel, Olivier Briand, Kadiombo Bantubungi, Sandrine Caron, Laure B. Bindels, Nathalie M. Delzenne, Anne Tailleux, Bart Staels, Sophie Lestavel
SCIENTIFIC REPORTS
(2020)
Article
Biology
Leslie Duplaquet, Catherine Leroy, Audrey Vinchent, Sonia Paget, Jonathan Lefebvre, Fabien Vanden Abeele, Steve Lancel, Florence Giffard, Rejane Paumelle, Gabriel Bidaux, Laurent Heliot, Laurent Poulain, Alessandro Furlan, David Tulasne
Article
Biochemistry & Molecular Biology
Vanessa Dubois, Celine Gheeraert, Wouter Vankrunkelsven, Julie Dubois-Chevalier, Helene Dehondt, Marie Bobowski-Gerard, Manjula Vinod, Francesco Paolo Zummo, Fabian Guiza, Maheul Ploton, Emilie Dorchies, Laurent Pineau, Alexis Boulinguiez, Emmanuelle Vallez, Eloise Woitrain, Eric Bauge, Fanny Lalloyer, Christian Duhem, Nabil Rabhi, Ronald E. van Kesteren, Cheng-Ming Chiang, Steve Lancel, Helene Duez, Jean-Sebastien Annicotte, Rejane Paumelle, Ilse Vanhorebeek, Greet Van den Berghe, Bart Staels, Philippe Lefebvre, Jerome Eeckhoute
MOLECULAR SYSTEMS BIOLOGY
(2020)
Article
Biology
Asma Ayari, Manuel Rosa-Calatrava, Steve Lancel, Johanna Barthelemy, Andres Pizzorno, Alicia Mayeuf-Louchart, Morgane Baron, David Hot, Lucie Deruyter, Daphnee Soulard, Thomas Julien, Christelle Faveeuw, Olivier Molendi-Coste, David Dombrowicz, Laura Sedano, Valentin Sencio, Ronan Le Goffic, Francois Trottein, Isabelle Wolowczuk
COMMUNICATIONS BIOLOGY
(2020)
Article
Biochemistry & Molecular Biology
Olivia May, Laure Yatime, Nicolas S. Merle, Florian Delguste, Mike Howsam, Marie Daugan, Charles Paul-Constant, Muriel Billamboz, Alina Ghinet, Steve Lancel, Jordan D. Dimitrov, Eric Boulanger, Lubka T. Roumenina, Marie Frimat
Summary: The interaction between RAGE and heme with micromolar affinity could potentially promote proinflammatory and prothrombotic signaling in vivo. This suggests that this interaction may play a role in heme-overload conditions.
Article
Geriatrics & Gerontology
Frederic N. Daussin, Eric Boulanger, Steve Lancel
Summary: Sarcopenia is characterized by muscle mass and function loss, with mitochondrial alterations considered a key contributor. The pro-inflammatory receptor RAGE is involved in inflammaging and may have a connection with mitochondria in controlling sarcopenia.
EXPERIMENTAL GERONTOLOGY
(2021)
Article
Cardiac & Cardiovascular Systems
Dominique Croteau, Ivan Luptak, Jordan M. Chambers, Ion Hobai, Marcello Panagia, David R. Pimentel, Deborah A. Siwik, Fuzhong Qin, Wilson S. Colucci
Summary: The study found that ertugliflozin not only prevented high-fat, high-sucrose-induced pathological cardiac remodeling, but also improved contractile reserve and induced the expression of oxidative phosphorylation and fatty acid metabolism gene sets independent of diabetic status.
JOURNAL OF THE AMERICAN HEART ASSOCIATION
(2021)
Article
Biochemistry & Molecular Biology
Victoriane Peugnet, Maggy Chwastyniak, Paul Mulder, Steve Lancel, Laurent Bultot, Natacha Fourny, Edith Renguet, Heiko Bugger, Olivia Beseme, Anne Loyens, Wilfried Heyse, Vincent Richard, Philippe Amouyel, Luc Bertrand, Florence Pinet, Emilie Dubois-Deruy
Summary: This study investigated the impact of mitochondria-targeted therapy on cardiac hypertrophy and found that MitoQ can reduce mitochondrial ROS and hypertrophy, but it may also affect mitochondrial structure and function by impairing mitochondrial respiration and mitophagy, particularly showing deleterious effects in cardiomyocytes.
Article
Medicine, Research & Experimental
Alexis Boulinguiez, Christian Duhem, Alicia Mayeuf-Louchart, Benoit Pourcet, Yasmine Sebti, Kateryna Kondratska, Valerie Montel, Stephane Delhaye, Quentin Thorel, Justine Beauchamp, Aurore Hebras, Marion Gimenez, Marie Couvelaere, Mathilde Zecchin, Lise Ferri, Natalia Prevarskaya, Anne Forand, Christel Gentil, Jessica Ohana, France Pietri-Rouxel, Bruno Bastide, Bart Staels, Helene Duez, Steve Lancel
Summary: The study shows that NR1D1 plays a crucial role in regulating skeletal muscle SR calcium homeostasis by repressing the expression of the SERCA inhibitor myoregulin. Lower NR1D1 expression is observed in patients with Duchenne muscular dystrophy, while pharmacological activation of NR1D1 improves calcium homeostasis and muscle structure and function.
Article
Biology
Alexandre Pierre, Claire Bourel, Raphael Favory, Benoit Brassart, Frederic Wallet, Frederic N. N. Daussin, Sylvain Normandin, Michael Howsam, Raphael Romien, Jeremy Lemaire, Gaelle Grolaux, Arthur Durand, Marie Frimat, Bruno Bastide, Philippe Amouyel, Eric Boulanger, Sebastien Preau, Steve Lancel
Summary: Sepsis is a life-threatening infection that leads to muscle weakness, which impairs short- and long-term prognoses. This study investigated the impact of an energy deficit on skeletal muscle during the early stages of sepsis. The results showed that a sepsis-like energy deficit did not explain the muscle fiber atrophy and mitochondrial dysfunction observed in sepsis, but led to specific metabolic adaptations not found in sepsis.