Review
Biochemistry & Molecular Biology
Tom Kretzschmar, Jasmine M. F. Wu, P. Christian Schulze
Summary: Heart failure remains the most common cause of death in the industrialized world, and despite new therapeutic interventions, complete prevention of its development and progression is still not possible, highlighting the need for further research to understand the underlying mechanisms. This review provides a detailed overview of the contribution of impaired mitochondrial dynamics and energy homeostasis during heart failure progression.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Biology
Christina Schenkl, Estelle Heyne, Torsten Doenst, Paul Christian Schulze, Tien Dung Nguyen
Summary: Despite advances in treating cardiac disorders, heart failure (HF) continues to increase globally and poses a medical and economic burden. HF is characterized by metabolic remodeling in the mitochondria, affecting energy homeostasis, calcium handling, oxidative stress, and inflammation. This study focuses on highlighting mitochondrial metabolic alterations and their impact on the pathophysiology of HF, as well as discussing potential metabolic approaches to improve cardiac function.
Review
Biochemistry & Molecular Biology
Haikel Dridi, Gaetano Santulli, Laith Bahlouli, Marco C. Miotto, Gunnar Weninger, Andrew R. Marks
Summary: Heart failure is a global health challenge characterized by defective calcium handling, mitochondrial calcium overload, and oxidative stress. Calcium not only regulates contraction in cardiomyocytes, but also affects mitochondrial metabolism and oxidative stress signaling. Understanding the mechanisms of mitochondrial calcium uptake and the regulation of increased calcium influx is crucial for identifying therapeutic targets for heart failure.
Review
Biochemistry & Molecular Biology
Daniele Mancardi, Mariarosa Mezzanotte, Elisa Arrigo, Alice Barinotti, Antonella Roetto
Summary: Iron accumulation can lead to impaired redox homeostasis and cell death, with ferroptosis being a form of cell death strictly dependent on iron and reactive oxygen species. The role of ferroptosis in organs like the heart and liver is still not fully understood, but it may play a crucial part in the pathogenesis of certain diseases.
Article
Cardiac & Cardiovascular Systems
Douglas J. Chapski, Maximilian Cabaj, Marco Morselli, Rosibel J. Mason, Elizabeth Soehalim, Shuxun Ren, Matteo Pellegrini, Yibin Wang, Thomas M. Vondriska, Manuel Rosa-Garrido
Summary: The study revealed that chromatin remodeling during early compensation after pathologic stimuli persists into the later decompensatory phases of heart failure. The findings provide insights into how local chromatin features govern gene expression within the context of global genomic structure and highlight chromatin remodeling events that could be targeted for therapeutic interventions in disease.
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
(2021)
Article
Cardiac & Cardiovascular Systems
Zoe Kwan, Binoy Paulose Nadappuram, Manton M. Leung, Sanika Mohagaonkar, Ao Li, Kumuthu S. Amaradasa, Ji Chen, Stephen Rothery, Iyobel Kibreab, Jiarong Fu, Jose L. Sanchez-Alonso, Catherine A. Mansfield, Hariharan Subramanian, Alexander Kondrashov, Peter T. Wright, Pamela Swiatlowska, Viacheslav O. Nikolaev, Beata Wojciak-Stothard, Aleksandar P. Ivanov, Joshua B. Edel, Julia Gorelik
Summary: The localization and function of beta-ARs in cardiac cells are regulated by selective trafficking of mRNA and localized translation, which is dependent on microtubules. Myocardial infarction and heart failure alter the localization pattern of beta-ARs, leading to impaired signaling.
CIRCULATION RESEARCH
(2023)
Review
Pharmacology & Pharmacy
Fabiana Passaro, Carlo Gabriele Tocchetti, Gaia Spinetti, Francesca Paudice, Luigi Ambrosone, Ciro Costagliola, Francesco Cacciatore, Pasquale Abete, Gianluca Testa
Summary: Heart failure is a clinical syndrome caused by cardiac structural and/or functional abnormalities, leading to reduced cardiac output and/or elevated intracardiac pressures. Nanoparticles can be used for targeted drug delivery to identify, prevent, and treat cardiac fibrosis.
ADVANCED DRUG DELIVERY REVIEWS
(2021)
Article
Cardiac & Cardiovascular Systems
William D. Watson, Peregrine G. Green, Andrew J. M. Lewis, Per Arvidsson, Giovanni Luigi De Maria, Hakan Arheden, Einar Heiberg, William T. Clarke, Christopher T. Rodgers, Ladislav Valkovic, Stefan Neubauer, Neil Herring, Oliver J. Rider
Summary: The study shows that even in nonischemic heart failure patients with severely impaired systolic function, the heart retains significant metabolic flexibility, including the ability to change substrate use to match arterial supply and workload changes. Increasing the uptake and oxidation of long-chain fatty acids is associated with improved myocardial energetics and contractility.
Article
Chemistry, Multidisciplinary
Ajit Magadum, Neha Singh, Ann Anu Kurian, Mohammad Tofael Kabir Sharkar, Nishat Sultana, Elena Chepurko, Keerat Kaur, Magdalena M. Zak, Yoav Hadas, Djamel Lebeche, Susmita Sahoo, Roger Hajjar, Lior Zangi
Summary: Heart failure remains a major issue globally, with cardiac hypertrophy and fibrosis being key factors. The regulator Pip4k2c, associated with mTORC1, plays a role in these processes. Studies show that deleting Pip4k2c does not affect embryonic cardiac development, but leads to increased rates of CH, CF, and sudden death in adult mice. Upregulating Pip4k2c improves heart function, reverses CH and CF, and enhances survival through inhibiting TGF beta 1 via specific pathways. Loss-and-gain-of-function studies identify Pip4k2c as a potential therapeutic target for CF, CH, and HF, utilizing modRNA as an effective gene therapy approach.
Review
Biology
Giampaolo Morciano, Veronica Angela Maria Vitto, Esmaa Bouhamida, Carlotta Giorgi, Paolo Pinton
Summary: The heart is crucial for the circulation of blood and oxygen in the body, and its function relies on a delicate balance of energy consumption and generation. Mitochondrial dysfunctions have been identified as key factors in the development of various heart diseases, particularly heart failure.
Article
Cardiac & Cardiovascular Systems
Andrew N. Carley, Santosh K. Maurya, Matthew Fasano, Yang Wang, Craig H. Selzman, Stavros G. Drakos, E. Douglas Lewandowski
Summary: The study revealed that short-chain fatty acids (SCFAs) are oxidized more readily than ketones in failing hearts, serving as a potential unexplored carbon source for energy production. Despite both SCFAs and ketones bypassing reduced CPT1 activity, SCFAs show higher oxidation rates and may represent a promising alternative energy substrate for failing hearts.
Article
Cardiac & Cardiovascular Systems
John C. Dykes, David N. Rosenthal, Daniel Bernstein, Doff B. McElhinney, Maryanne R. K. Chrisant, Kevin P. Daly, Rebecca K. Ameduri, Kenneth Knecht, Marc E. Richmond, Kimberly Y. Lin, Simon Urschel, Jacob Simmonds, Kathleen E. Simpson, Erin L. Albers, Asma Khan, Kurt Schumacher, Christopher S. Almond, Sharon Chen
Summary: This study aimed to describe the clinical and hemodynamic characteristics of Fontan failure in children listed for heart transplant. The results showed that elevated Fontan pressure is more common than low cardiac output in pediatric failing Fontan patients, and there are subtle hemodynamic differences between the various phenotypes of Fontan failure in children. Additionally, waitlist and post-transplant mortality risks differ by phenotype.
JOURNAL OF HEART AND LUNG TRANSPLANTATION
(2021)
Article
Cardiac & Cardiovascular Systems
Nobuyuki Enzan, Shouji Matsushima, Soichiro Ikeda, Kosuke Okabe, Akihito Ishikita, Taishi Yamamoto, Masashi Sada, Ryo Miyake, Yoshitomo Tsutsui, Ryohei Nishimura, Takayuki Toyohara, Yuki Ikeda, Yoko Shojima, Hiroko Deguchi Miyamoto, Tomonori Tadokoro, Masataka Ikeda, Kohtaro Abe, Tomomi Ide, Shintaro Kinugawa, Hiroyuki Tsutsui
Summary: This study reveals that ZBP1 knockdown exacerbates mtDNA-induced inflammation in cardiomyocytes by increasing RIPK3, NF-kappa B, NLRP3, IL-1 beta, and IL-6 expression. In mouse models of myocardial infarction and heart failure, ZBP1 knockout worsens left ventricular dilatation and dysfunction, accompanied by increased expression of RIPK3, NF-kappa B, NLRP3, IL-1 beta, and IL-6. This suggests that ZBP1 acts as an endogenous suppressor of mtDNA-induced myocardial inflammation and plays a protective role against cardiac remodeling.
CIRCULATION RESEARCH
(2023)
Article
Cardiac & Cardiovascular Systems
Kyra K. Peczkowski, Mohammed A. Mashali, Nancy S. Saad, Austin Hare, Courtney M. Campbell, Bryan A. Whitson, Nahush A. Mokadam, Paul M. L. Janssen
Summary: The study found that nonfailing hearts generally have higher EAT content compared to end-stage failing hearts, and there is no strong correlation between EAT quantity and BMI in both nonfailing and failing hearts. Atrial EAT is closely correlated with ventricular EAT in both nonfailing and failing hearts.
JOURNAL OF THE AMERICAN HEART ASSOCIATION
(2022)
Article
Multidisciplinary Sciences
Anna Borowiec, Patrycja Ozdowska, Magdalena Rosinska, Agnieszka Jagiello-Gruszfeld, Slawomir Jasek, Joanna Waniewska, Beata Kotowicz, Hanna Kosela-Paterczyk, Elzbieta Lampka, Agata Makowka, Malgorzata Fuksiewicz, Magdalena Chojnacka, Agnieszka Zebrowska, Katarzyna Gepner, Aleksandra Kapala, Andrzej Cieszanowski, Zbigniew Nowecki, Jan Walewski
Summary: This study aims to assess the prognostic value of coronary atherosclerosis burden and CAC score on the onset of cardiac dysfunction associated with cancer therapy. It will include 80 cancer patients who will undergo coronary computed tomographic angiography before high-dose chemotherapy and be followed up for 12 months. The occurrence of cancer therapy-related cardiovascular toxicity will be evaluated, and new biomarkers of atherosclerosis will be measured.