Article
Cardiac & Cardiovascular Systems
Yijun Yang, Justin Kurian, Giana Schena, Jaslyn Johnson, Hajime Kubo, Joshua G. Travers, Chunya Kang, Anna Maria Lucchese, Deborah M. Eaton, Maoting Lv, Na Li, Lorianna G. Leynes, Daohai Yu, Fengzhen Yang, Timothy A. McKinsey, Raj Kishore, Mohsin Khan, Sadia Mohsin, Steven R. Houser
Summary: The study suggests that metabolic syndrome in obese pregnant women may lead to pathological cardiac remodeling, increasing the risk of chronic heart disorders.
Article
Biochemistry & Molecular Biology
Stephanie Bettink, Jan-Christian Reil, Andrey Kazakov, Christina Koerbel, Dominic Millenaar, Ulrich Laufs, Bruno Scheller, Michael Boehm, Stephan H. Schirmer
Summary: TRIF plays a significant role in pressure-overload-induced cardiac hypertrophy. It regulates the release of inflammatory cytokines and accumulation of inflammatory cells, and is involved in the development of cardiac fibrosis.
Article
Biochemistry & Molecular Biology
Agnieszka A. Gorska, Clara Sandmann, Eva Riechert, Christoph Hofmann, Ellen Malovrh, Eshita Varma, Vivien Kmietczyk, Julie Oelschlaeger, Lonny Juergensen, Verena Kamuf-Schenk, Claudia Stroh, Jennifer Furkel, Mathias H. Konstandin, Carsten Sticht, Etienne Boileau, Christoph Dieterich, Norbert Frey, Hugo A. Katus, Shirin Doroudgar, Mirko Voelkers
Summary: The study reveals the role of mTOR in pathological remodeling of the heart, showing that it protects cardiomyocytes by controlling the translation of specific genes, with Cand2 being a mTOR-regulated protective gene.
Article
Cell Biology
Jennifer L. Rodgers, Sahit Vanthenapalli, Siva K. Panguluri
Summary: Clinical reports show high ICU mortality when hyperoxia is used during mechanical ventilation. This study on mice reveals that hyperoxia treatment leads to body weight reduction and increased cardiomyocyte size at 24 hours, followed by arrhythmias and worsened cardiac dysfunction at 48 and 72 hours. Electrical remodeling precedes structural remodeling and worsens with longer hyperoxia exposure.
JOURNAL OF CELLULAR PHYSIOLOGY
(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
Cardiac & Cardiovascular Systems
Giovanni E. Davogustto, Rebecca L. Salazar, Hernan G. Vasquez, Anja Karlstaedt, William P. Dillon, Patrick H. Guthrie, Joseph R. Martin, Heidi Vitrac, Gina De La Guardia, Deborah Vela, Aleix Ribas-Latre, Corrine Baumgartner, Kristin Eckel-Mahan, Heinrich Taegtmeyer
Summary: Activating mTORC1 in the adult heart triggers a non-specific form of hypertrophy, preceded by changes in cardiac glucose metabolism.
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
(2021)
Article
Medicine, Research & Experimental
Lavinia Rech, Mahmoud Abdellatif, Verena Stangl, Nishani Mabotuwana, Sean Hardy, Peter P. Rainer, Maria Poettler
Summary: This study investigated the protective effects of pharmacologic STING inhibition after myocardial infarction. The results showed that pharmacologic STING inhibition can reduce infarct expansion and scarring, improve left ventricular systolic function, and attenuate myocardial hypertrophy. This suggests that selective small-molecule STING inhibition has the potential to improve wound healing responses and pathological remodeling after myocardial infarction.
Review
Cardiac & Cardiovascular Systems
Xing-Huai Huang, Jia-Lu Li, Xin-Yue Li, Shu-Xia Wang, Zhi-Han Jiao, Si-Qi Li, Jun Liu, Jian Ding
Summary: miR-208a plays a key role in regulating heart development and function, and is involved in cardiac pathogenesis, conduction system regulation, myofiber gene expression, and systemic energy homeostasis. Despite its critical functions, the regulatory networks involving miR-208a are still not fully understood, and further research is needed to clarify its diverse and potentially opposite roles in different molecular contexts.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2021)
Article
Cardiac & Cardiovascular Systems
Binh Y. Nguyen, Fangchao Zhou, Pablo Binder, Wei Liu, Susanne S. Hille, Xiaojing Luo, Min Zi, Hongyuan Zhang, Antony Adamson, Fozia Z. Ahmed, Sam Butterworth, Elizabeth J. Cartwright, Oliver J. Mueller, Kaomei Guan, Elizabeth M. Fitzgerald, Xin Wang
Summary: This study demonstrates that prolylcarboxylpeptidase has a protective effect on the heart by controlling myocardial angiotensin II levels, which can alleviate angiotensin II-induced hypertrophic remodeling and fibrosis. Furthermore, the combination of prolylcarboxylpeptidase overexpression and the antihypertensive drug losartan provides more effective protection against angiotensin II-induced cardiac dysfunction.
JOURNAL OF THE AMERICAN HEART ASSOCIATION
(2023)
Article
Physiology
C. Ruperez, A. Blasco-Roset, D. Kular, M. Cairo, G. Ferrer-Curriu, J. Villarroya, M. Zamora, F. Crispi, F. Villarroya, A. Planavila
Summary: This study investigates the reversibility of cold-induced cardiac hypertrophy and the role of autophagy in this process. The results show that exposure to cold leads to cardiac hypertrophy in mice, but this hypertrophy is fully reversed after 1 week of deacclimation. Autophagy is proposed as a major mechanism underlying the heart remodeling seen in response to cold exposure and its posterior reversion after deacclimation.
FRONTIERS IN PHYSIOLOGY
(2022)
Article
Pharmacology & Pharmacy
Frederic Boal, Mathieu Cinato, Andrei Timotin, Heike Muenzberg, Emily Qualls-Creekmore, Solomiia Kramar, Halyna Loi, Jerome Roncalli, Sokhna Keita, Helene Tronchere, Oksana Kunduzova
Summary: The regulatory peptide galanin plays an important role in the heart, with GalR2 identified as the predominant receptor subtype in adult mouse hearts. Suppression of GalR2 gene promotes cardiac hypertrophy, fibrosis, and mitochondrial oxidative stress. In vitro experiments have shown that silencing GalR2 affects the effects of galanin on cells.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Jun H. Heo, Sang R. Lee, Seong Lae Jo, Hyun Yang, Hye Won Lee, Eui-Ju Hong
Summary: Letrozole, an aromatase inhibitor used in breast cancer treatment, has been reported to cause metabolic changes and structural remodeling in the heart. Our study found that letrozole exposure in female rats resulted in decreased fatty acid oxidation, increased glycolysis, and left ventricular hypertrophy. This shift in cardiac metabolism may lead to reduced energy supply and increased risk of heart failure.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Cell Biology
Vanessa P. Teixeira, Kiany Miranda, Sergio Scalzo, Cibele Rocha-Resende, Mario Morais Silva, Geisa C. S. V. Tezini, Marcos B. Melo, Fernando Pedro Souza-Neto, Kaoma S. C. Silva, Itamar C. G. Jesus, Anderson K. Santos, Mauro de Oliveira, Raphael E. Szawka, Helio C. Salgado, Marco Antonio Maximo Prado, Maristela O. Poletini, Silvia Guatimosim
Summary: In this study, it was found that enhanced cholinergic signaling in mice leads to cardiac dilation and failure under conditions of reduced estrogen levels. Treatment with 17 beta-estradiol was able to normalize cardiac parameters in the mice, suggesting a link between estrogen status and cardiac response in this model.
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
(2021)
Article
Genetics & Heredity
Chenxi Zhu, Zhehao Piao, Li Jin
Summary: HDAC5 may suppress the activation of the ERK/EGR1 signaling pathway to regulate MEF2A expression and participate in cardiac pathophysiology.
ORPHANET JOURNAL OF RARE DISEASES
(2023)
Review
Biochemistry & Molecular Biology
Annika-Ricarda Kuhn, Marc van Bilsen
Summary: Heart failure is associated with changes in cardiac intermediary metabolism, but the role of metabolic remodeling in heart failure remains unclear. Recent research in cancer has shown that metabolic rewiring directly affects cellular phenotype and function, and similar functions may be served by the rewiring of cardiac cellular metabolism in heart failure. This review discusses the impact of metabolic pathways on cellular phenotype in different cell types of the heart and evaluates their relevance for cardiac pathogenesis and therapy.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
