Journals Journal of Molecular and Cellu...

Journal of Molecular and Cellular Cardiology
Caterina Redwanz, Ricardo H Pires, Doreen Biedenweg, Stefan Groß, Oliver Otto, Stephanie Könemann
A better understanding of the underlying pathomechanisms of diastolic dysfunction is crucial for the development of targeted therapeutic options with the aim to increase the patients' quality of life. In order to shed light on the processes involved, suitable models are required. Here, effects of endothelin-1 (ET-1) treatment on cardiomyocytes derived from human induced pluripotent stem cells (hiPSCs) were investigated. While it is well established, that ET-1 treatment induces hypertrophy in cardiomyocytes, resulting changes in cell mechanics and contractile behavior with focus on relaxation have not been examined before...
July 15, 2024: Journal of Molecular and Cellular Cardiology
Weixiao Chen, Ai Chen, Guili Lian, Yan Yan, Junping Liu, Jingying Wu, Gufeng Gao, Liangdi Xie
Pulmonary hypertension (PH) is characterized by excessive proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs), in which inflammatory signaling caused by activation of the NF-κB pathway plays an important role. A20 is an important negative regulator of the NF-κB pathway, and zinc promotes the expression of A20 and exerts a protective effect against various diseases (e.g. COVID19) by inhibiting the inflammatory signaling. The role of A20 and intracellular zinc signaling in PH has been explored, but the extracellular zinc signaling is not well understood, and whether zinc has protective effects on PH is still elusive...
July 11, 2024: Journal of Molecular and Cellular Cardiology
Selina M Tucker, Salman I Essajee, Cooper M Warne, Gregory M Dick, Michael P Heard, Nicole Crowe, Styliani Goulopoulou, Johnathan D Tune
Understanding of the mechanisms contributing to the increased maternal susceptibility for major adverse cardiovascular events in the postpartum period remains poor. Accordingly, this study tested the hypothesis that the balance between coronary blood flow and myocardial metabolism is compromised during the puerperium period (35-45 days post-delivery) in swine. Systemic and coronary hemodynamic responses were assessed in anesthetized, open-chest control (nonpregnant) and puerperium/postpartum swine at baseline and in response to intravenous infusion of dobutamine (1-30 μg/kg/min)...
July 3, 2024: Journal of Molecular and Cellular Cardiology
Lisa K McClendon, Rainer B Lanz, Anil Panigrahi, Kristan Gomez, Michael J Bolt, Min Liu, Fabio Stossi, Michael A Mancini, Clifford C Dacso, David M Lonard, Bert W O'Malley
We recently discovered that steroid receptor coactivators (SRCs) SRCs-1, 2 and 3, are abundantly expressed in cardiac fibroblasts (CFs) and their activation with the SRC small molecule stimulator MCB-613 improves cardiac function and dramatically lowers pro-fibrotic signaling in CFs post-myocardial infarction. These findings suggest that CF-derived SRC activation could be beneficial in the mitigation of chronic heart failure after ischemic insult. However, the cardioprotective mechanisms by which CFs contribute to cardiac pathological remodeling are unclear...
July 3, 2024: Journal of Molecular and Cellular Cardiology
Satadru K Lahiri, Jiao Lu, Yuriana Aguilar-Sanchez, Hui Li, Lucia M Moreira, Mohit M Hulsurkar, Arielys Mendoza, Mara R Turkieltaub Paredes, Jose Alberto Navarro-Garcia, Elda Munivez, Brooke Horist, Oliver M Moore, Gunnar Weninger, Sören Brandenburg, Christof Lenz, Stephan E Lehnart, Rana Sayeed, George Krasopoulos, Vivek Srivastava, Lilei Zhang, Jason M Karch, Svetlana Reilly, Xander H T Wehrens
Coronary heart disease (CHD) is a prevalent cardiac disease that causes over 370,000 deaths annually in the USA. In CHD, occlusion of a coronary artery causes ischemia of the cardiac muscle, which results in myocardial infarction (MI). Junctophilin-2 (JPH2) is a membrane protein that ensures efficient calcium handling and proper excitation-contraction coupling. Studies have identified loss of JPH2 due to calpain-mediated proteolysis as a key pathogenic event in ischemia-induced heart failure (HF). Our findings show that calpain-2-mediated JPH2 cleavage yields increased levels of a C-terminal cleaved peptide (JPH2-CTP) in patients with ischemic cardiomyopathy and mice with experimental MI...
July 1, 2024: Journal of Molecular and Cellular Cardiology
Michal Pásek, Markéta Bébarová, Milena Šimurdová, Jiří Šimurda
The sarcolemmal Ca2+ efflux pathways, Na+ -Ca2+ -exchanger (NCX) and Ca2+ -ATPase (PMCA), play a crucial role in the regulation of intracellular Ca2+ load and Ca2+ transient in cardiomyocytes. The distribution of these pathways between the t-tubular and surface membrane of ventricular cardiomyocytes varies between species and is not clear in human. Moreover, several studies suggest that this distribution changes during the development and heart diseases. However, the consequences of NCX and PMCA redistribution in human ventricular cardiomyocytes have not yet been elucidated...
July 1, 2024: Journal of Molecular and Cellular Cardiology
Yutong Li, Xiang Wang, Yaguang Bi, Mengjiao Zhang, Weidong Xiong, Xiaolong Hu, Yingmei Zhang, Fei He
BACKGROUNDS: Pathological cardiac hypertrophy is considered one of the independent risk factors for heart failure, with a rather complex pathogenic machinery. Sorting nexins (SNXs), denoting a diverse family of cytoplasmic- and membrane-associated phosphoinositide-binding proteins, act as a pharmacological target against specific cardiovascular diseases including heart failure. Family member SNX5 was reported to play a pivotal role in a variety of biological processes. However, contribution of SNX5 to the development of cardiac hypertrophy, remains unclear...
June 29, 2024: Journal of Molecular and Cellular Cardiology
Zachary J Williams, Anita Alvarez-Laviada, Daniel Hoagland, L Jane Jourdan, Steven Poelzing, Julia Gorelik, Robert G Gourdie
Cardiac arrhythmia treatment is a clinical challenge necessitating safer and more effective therapies. Recent studies have highlighted the role of the perinexus, an intercalated disc nanodomain enriched in voltage-gated sodium channels including both Nav 1.5 and β1 subunits, adjacent to gap junctions. These findings offer insights into action potential conduction in the heart. A 19-amino acid SCN1B (β1/β1B) mimetic peptide, βadp1, disrupts VGSC beta subunit-mediated adhesion in cardiac perinexii, inducing arrhythmogenic changes...
June 26, 2024: Journal of Molecular and Cellular Cardiology
Adnan Shaaban, Shane S Scott, Ashley N Greenlee, Nkongho Binda, Ali Noor, Averie Webb, Shuliang Guo, Najhee Purdy, Nicholas Pennza, Alma Habib, Somayya J Mohammad, Sakima A Smith
Atrial fibrillation (AF) is a common arrhythmic complication in cancer patients and can be exacerbated by traditional cytotoxic and targeted anticancer therapies. Increased incidence of AF in cancer patients is independent of confounding factors, including preexisting myocardial arrhythmogenic substrates, type of cancer, or cancer stage. Mechanistically, AF is characterized by fast unsynchronized atrial contractions with rapid ventricular response, which impairs ventricular filling and results in various symptoms such as fatigue, chest pain, and shortness of breath...
June 17, 2024: Journal of Molecular and Cellular Cardiology
John E Madias
No abstract text is available yet for this article.
June 17, 2024: Journal of Molecular and Cellular Cardiology
Diego Quiroga, Barbara Roman, Marwan Salih, William N Daccarett-Bojanini, Haley Garbus, Obialunanma V Ebenebe, Jeffrey M Dodd-O, Brian O'Rourke, Mark Kohr, Samarjit Das
Obesity-induced cardiac dysfunction is growing at an alarming rate, showing a dramatic increase in global prevalence. Mitochondrial translocation of miR-181c in cardiomyocytes results in excessive reactive oxygen species (ROS) production during obesity. ROS causes Sp1, a transcription factor for MICU1, to be degraded via post-translational modification. The subsequent decrease in MICU1 expression causes mitochondrial Ca2+ accumulation, ultimately leading to a propensity for heart failure. Herein, we hypothesized that phosphorylation of Argonaute 2 (AGO2) at Ser 387 (in human) or Ser 388 (in mouse) inhibits the translocation of miR-181c into the mitochondria by increasing the cytoplasmic stability of the RNA-induced silencing complex (RISC)...
June 14, 2024: Journal of Molecular and Cellular Cardiology
Khaja Shameem Mohammed Abdul, Kimin Han, Alyssa B Guerrero, Cekia N Wilson, Amogh Kulkarni, Nicole H Purcell
Nicotine, a key constituent of tobacco/electronic cigarettes causes cardiovascular injury and mortality. Nicotine is known to induce oxidative stress and mitochondrial dysfunction in cardiomyocytes leading to cell death. However, the underlying mechanisms remain unclear. Pleckstrin homology domain leucine-rich repeat protein phosphatase (PHLPP) is a member of metal-dependent protein phosphatase (PPM) family and is known to dephosphorylate several AGC family kinases and thereby regulate a diverse set of cellular functions including cell growth, survival, and death...
June 6, 2024: Journal of Molecular and Cellular Cardiology
Nikolay Naumenko, Jussi T Koivumäki, Olesia Lunko, Tomi Tuomainen, Robert Leigh, Mina Rabie, Jalmari Laurila, Minna Oksanen, Sarka Lehtonen, Jari Koistinaho, Pasi Tavi
Mutations in ubiquitously expressed presenilin genes (PSENs) lead to early-onset familial Alzheimer's disease (FAD), but patients carrying the mutation also suffer from heart diseases. To elucidate the cardiac myocyte specific effects of PSEN ΔE9, we studied cardiomyocytes derived from induced pluripotent stem cells (iPSC-CMs) from patients carrying AD-causing PSEN1 exon 9 deletion (PSEN1 ΔE9). When compared with their isogenic controls, PSEN1 ΔE9 cardiomyocytes showed increased sarcoplasmic reticulum (SR) Ca2+ leak that was resistant to blockage of ryanodine receptors (RyRs) by tetracaine or inositol-3-reseceptors (IP3 Rs) by 2-ABP...
June 6, 2024: Journal of Molecular and Cellular Cardiology
Yasunori Abe, Amarsanaa Javkhlant, Joshua M Spin, Kensuke Toyama
No abstract text is available yet for this article.
June 5, 2024: Journal of Molecular and Cellular Cardiology
Gopika SenthilKumar, Stephen T Hammond, Zachary Zirgibel, Katie E Cohen, Andreas M Beyer, Julie K Freed
An increasing body of evidence suggests a pivotal role for the microvasculature in the development of cardiovascular disease. A dysfunctional coronary microvascular network, specifically within endothelial cells-the inner most cell layer of vessels-is considered a strong, independent risk factor for future major adverse cardiac events. However, challenges exist with evaluating this critical vascular bed, as many of the currently available techniques are highly invasive and cost prohibitive. The more easily accessible peripheral microcirculation has surfaced as a potential surrogate in which to study mechanisms of coronary microvascular dysfunction and likewise may be used to predict poor cardiovascular outcomes...
June 5, 2024: Journal of Molecular and Cellular Cardiology
Xiao-Min Li, Zi-Jun Wu, Jun-Yu Fan, Man-Qi Liu, Chu-Ge Song, Hong-Qiao Chen, Yu Yin, Ao Li, Ya-Hong Wang, Sheng-Lan Gao, Zhi-Liang Xu, Gang Liu, Keng Wu
Diabetic cardiomyopathy (DCM) is a heart failure syndrome, and is one of the major causes of morbidity and mortality in diabetes. DCM is mainly characterized by ventricular dilation, myocardial hypertrophy, myocardial fibrosis and cardiac dysfunction. Clinical studies have found that insulin resistance is an independent risk factor for DCM. However, its specific mechanism of DCM remains unclear. 8-hydroxyguanine DNA glycosylase 1(OGG1)is involved in DNA base repair and the regulation of inflammatory genes. In this study, we show that OGG1 was associated with the occurrence of DCM...
June 4, 2024: Journal of Molecular and Cellular Cardiology
Giovanni Maroli, Anne Schänzer, Stefan Günther, Claudia Garcia-Gonzalez, Stefan Rupp, Hannah Schlierbach, Yanpu Chen, Johannes Graumann, Astrid Wietelmann, Johnny Kim, Thomas Braun
The HSP70 co-chaperone BAG3 targets unfolded proteins to degradation via chaperone assisted selective autophagy (CASA), thereby playing pivotal roles in the proteostasis of adult cardiomyocytes (CMs). However, the complex functions of BAG3 for regulating autophagy in cardiac disease are not completely understood. Here, we demonstrate that conditional inactivation of Bag3 in murine CMs leads to age-dependent dysregulation of autophagy, associated with progressive cardiomyopathy. Surprisingly, Bag3-deficient CMs show increased canonical and non-canonical autophagic flux in the juvenile period when first signs of cardiac dysfunction appear, but reduced autophagy during later stages of the disease...
June 3, 2024: Journal of Molecular and Cellular Cardiology
Michael W Lim, Jonathan M Kalman
Atrial fibrillation (AF), with its significant associated morbidity and mortality contributes to significant healthcare utilisation and expenditure. Given its progressively rising incidence, strategies to limit AF development and progression are urgently needed. Lifestyle modification is a potentially potent but underutilised weapon against the AF epidemic. The purpose of this article is to review the role of lifestyle factors as risk factors for AF, outline potential mechanisms of pathogenesis and examine the available evidence for lifestyle intervention in primary and secondary AF prevention...
June 3, 2024: Journal of Molecular and Cellular Cardiology
Ning Gu, Youcheng Shen, Yuanjie He, Chaofu Li, Weidong Xiong, Yiqing Hu, Zhimei Qiu, Fengli Peng, Weiyu Han, Chaozhong Li, Xianping Long, Ranzun Zhao, Yongchao Zhao, Bei Shi
BACKGROUND: Hypoxia-induced pulmonary artery hypertension (HPH) is a complication of chronic hypoxic lung disease and the third most common type of pulmonary artery hypertension (PAH). Epigenetic mechanisms play essential roles in the pathogenesis of HPH. N6-methyladenosine (m6A) is an important modified RNA nucleotide involved in a variety of biological processes and an important regulator of epigenetic processes. To date, the precise role of m6A and regulatory molecules in HPH remains unclear...
May 29, 2024: Journal of Molecular and Cellular Cardiology
Roman Y Medvedev, Saheed O Afolabi, Daniel G P Turner, Alexey V Glukhov
Atrial fibrillation (AF) is the most common cardiac rhythm disorder, often occurring in the setting of atrial distension 4and elevated myocardial stretch. While various mechano-electrochemical signal transduction pathways have been linked to AF development and progression, the underlying molecular mechanisms remain poorly understood, hampering AF therapies. In this review, we describe different aspects of stretch-induced electro-anatomical remodeling as seen in animal models and in patients with AF. Specifically, we focus on cellular and molecular mechanisms that are responsible for mechano-electrochemical signal transduction and the development of ectopic beats triggering AF from pulmonary veins, the most common source of paroxysmal AF...
May 24, 2024: Journal of Molecular and Cellular Cardiology
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