YTHDF1 is pivotal for maintenance of cardiac homeostasis
The YTH-domain family (YTHDF) of RNA binding proteins can control gene expression at the post-transcriptional level by regulating mRNAs with N6-methyladenosine (m6A) modifications. Despite the established importance of m6A in the heart, the cardiac role of specific m6A-binding proteins remains unclear. Here, we characterized the function of YTHDF1 in cardiomyocytes using a newly generated cardiac-restricted mouse model. Deletion of YTHDF1 in adult cardiomyocytes led to hypertrophy, fibrosis, and dysfunction. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - May 18, 2024 Category: Cytology Authors: Volha A. Golubeva, Anindhya Sundar Das, Charles P. Rabolli, Lisa E. Dorn, Jop H. van Berlo, Federica Accornero Source Type: research

Cracking the code of the cardiovascular enigma: hPSC-derived endothelial cells unveil the secrets of endothelial dysfunction
Endothelial dysfunction is a central contributor to the development of most cardiovascular diseases and is characterised by the reduced synthesis or bioavailability of the vasodilator nitric oxide together with other abnormalities such as inflammation, senescence, and oxidative stress. The use of patient-specific and genome-edited human pluripotent stem cell-derived endothelial cells (hPSC-ECs) has shed novel insights into the role of endothelial dysfunction in cardiovascular diseases with strong genetic components such as genetic cardiomyopathies and pulmonary arterial hypertension. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - May 16, 2024 Category: Cytology Authors: Fedir N. Kiskin, Yuan Yang, Hao Yang, Joe Z. Zhang Tags: Review article Source Type: research

Knockdown of LncRNA Lcn2-204 alleviates sepsis-induced myocardial injury by regulation of iron overload and ferroptosis
Ferroptosis is an iron-dependent programmed cell death form resulting from lipid peroxidation damage, it plays a key role in organ damage and tumor development from various causes. Sepsis leads to severe host response after infection with high mortality. The long non-coding RNAs (LncRNAs) are involved in different pathophysiological mechanisms of multiple diseases. Here, we used cecal ligation and puncture (CLP) operation to mimic sepsis induced myocardial injury (SIMI) in mouse model, and LncRNAs and mRNAs were profiled by Arraystar mouse LncRNA Array V3.0. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - May 15, 2024 Category: Cytology Authors: Yuhui Huang, Lu Li, Yuping Li, Na Lu, Hongqian Qin, Rui Wang, Wentao Li, Zhipeng Cheng, Zhenghong Li, Pinfang Kang, Hongwei Ye, Qin Gao Source Type: research

Integrated modeling and simulation of recruitment of myocardial perfusion and oxygen delivery in exercise
This study uses a simulation and modeling approach to explore the mechanisms underlying the recruitment of myocardial perfusion and oxygen delivery in exercise. The simulation approach integrates model components representing: whole-body cardiovascular hemodynamics, cardiac mechanics and myocardial work; myocardial perfusion; and myocardial oxygen transport. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - May 14, 2024 Category: Cytology Authors: Victoria E. Sturgess, Johnathan D. Tune, C. Alberto Figueroa, Brian E. Carlson, Daniel A. Beard Source Type: research

Expanding landscape of coronary microvascular disease in co-morbid conditions: Metabolic disease and beyond
Coronary microvascular disease (CMD) and impaired coronary blood flow control are defects that occur early in the pathogenesis of heart failure in cardiometabolic conditions, prior to the onset of atherosclerosis. In fact, recent studies have shown that CMD is an independent predictor of cardiac morbidity and mortality in patients with obesity and metabolic disease. CMD is comprised of functional, structural, and mechanical impairments that synergize and ultimately reduce coronary blood flow in metabolic disease and in other co-morbid conditions, including transplant, autoimmune disorders, chemotherapy-induced cardiotoxici...
Source: Journal of Molecular and Cellular Cardiology - May 9, 2024 Category: Cytology Authors: Patricia E. McCallinhart, Alejandro R. Chade, Shawn B. Bender, Aaron J. Trask Tags: Review article Source Type: research

Persistent transcriptional changes in cardiac adaptive immune cells following myocardial infarction: New evidence from the re-analysis of publicly available single cell and nuclei RNA-sequencing data sets
Chronic immunopathology contributes to the development of heart failure after a myocardial infarction. Both T and B cells of the adaptive immune system are present in the myocardium and have been suggested to be involved in post-MI immunopathology. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - May 9, 2024 Category: Cytology Authors: Natasha de Winter, Jiahui Ji, Amalia Sintou, Elvira Forte, Michael Lee, Michela Noseda, Aoxue Li, Andrew L. Koenig, Kory Lavine, Sikander Hayat, Nadia Rosenthal, Costanza Emanueli, Prashant Srivastava, Susanne Sattler Source Type: research

Ferrostatin-1 specifically targets mitochondrial iron-sulfur clusters and aconitase to improve cardiac function in Sirtuin 3 cardiomyocyte knockout mice
In this study, we tested whether the knockout of SIRT3 in cardiomyocytes (SIRT3cKO) promotes mitochondrial ferroptosis and whether the blockade of ferroptosis would ameliorate mitochondrial dysfunction. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - May 9, 2024 Category: Cytology Authors: Aubrey C. Cantrell, Jessie Besanson, Quinesha Williams, Ngoc Hoang, Kristin Edwards, G. Reid Bishop, Yingjie Chen, Heng Zeng, Jian-Xiong Chen Source Type: research

Single-cell sequencing reveals the impact of endothelial cell PIEZO1 expression on thoracic aortic aneurysm
Thoracic aortic aneurysm (TAA) is a severe vascular disease that threatens human life, characterized by focal dilatation of the entire aortic wall, with a diameter 1.5 times larger than normal. PIEZO1, a mechanosensitive cationic channel, monitors mechanical stimulations in the environment, transduces mechanical signals into electrical signals, and converts them into biological signals to activate intracellular signaling pathways. However, the role of PIEZO1 in TAA is still unclear. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - May 7, 2024 Category: Cytology Authors: Xiaoyue Xiao, Hao Liu, Junhao Wan, Peiwen Yang, Zhiyue Xu, Shilin Wang, Qiang Guo, Shanshan Chen, Ping Ye, Sihua Wang, Jiahong Xia Source Type: research

Epicardial SMARCA4 deletion exacerbates cardiac injury in myocardial infarction and is related to the inhibition of epicardial epithelial-mesenchymal transition
This study found that SMARCA4 was activated over time in epicardial cells following MI, and some of activated cells belonged to downstream differentiation types of EPDCs. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - May 6, 2024 Category: Cytology Authors: Xingyu Ma, Jianjun Zhao, Yi Feng Source Type: research

Early matrix softening contributes to vascular smooth muscle cell phenotype switching and aortic dissection through down-regulation of microRNA-143/145
Thoracic aortic dissection (TAD) is characterised by extracellular matrix (ECM) dysregulation. Aberrations in the ECM stiffness can lead to changes in cellular functions. However, the mechanism by which ECM softening regulates vascular smooth muscle cell (VSMCs) phenotype switching remains unclear. To understand this mechanism, we cultured VSMCs in a soft extracellular matrix and discovered that the expression of microRNA (miR)-143/145, mediated by activation of the AKT signalling pathway, decreased significantly. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - May 6, 2024 Category: Cytology Authors: Zhaofei Ye, Shuolin Zhu, Guoqi Li, Jie Lu, Shan Huang, Jie Du, Yihui Shao, Zhili Ji, Ping Li Source Type: research

Exercise-induced changes in myocardial glucose utilization during periods of active cardiac growth
In this study, we used a dietary, in vivo isotope labeling approach to examine how exercise training influences the metabolic fate of carbon derived from dietary glucose in the heart during acute, active, and established phases of exercise-induced cardiac growth. Male and female FVB/NJ mice were subjected to treadmill running for up to 4  weeks and cardiac growth was assessed by gravimetry. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - May 3, 2024 Category: Cytology Authors: Kyle L. Fulghum, Helen E. Collins, Pawel K. Lorkiewicz, Teresa A. Cassel, Teresa W.M. Fan, Bradford G. Hill Source Type: research

ZFP36L1 controls KLF16 mRNA stability in vascular smooth muscle cells during restenosis after vascular injury
This study aimed to evaluate the role of ZFP36L1 in restenosis. We found that the expression of ZFP36L1 was inhibited in VSMC-phenotypic transformation induced by TGF- β, PDGF-BB, and FBS and also in the rat carotid injury model. In addition, we found that the overexpression of ZFP36L1 inhibited the proliferation and migration of VSMCs and promoted the expression of VSMC contractile genes; whereas ZFP36L1 interference promoted the proliferation and migration of V SMCs and suppressed the expression of contractile genes. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - April 21, 2024 Category: Cytology Authors: Ningheng Chen, Shiyong Wu, Kangkang Zhi, Xiaoping Zhang, Xueli Guo Source Type: research

MYBPC3-c.772G > A mutation results in haploinsufficiency and altered myosin cycling kinetics in a patient induced stem cell derived cardiomyocyte model of hypertrophic cardiomyopathy
Approximately 40% of hypertrophic cardiomyopathy (HCM) mutations are linked to the sarcomere protein cardiac myosin binding protein-C (cMyBP-C). These mutations are either classified as missense mutations or truncation mutations. One mutation whose nature has been inconsistently reported in the literature is the MYBPC3-c.772G  > A mutation. Using patient-derived human induced pluripotent stem cells differentiated to cardiomyocytes (hiPSC-CMs), we have performed a mechanistic study of the structure-function relationship for this MYBPC3-c.772G > A mutation versus a mutation corrected, isogenic cell line. (Source: Journal...
Source: Journal of Molecular and Cellular Cardiology - April 20, 2024 Category: Cytology Authors: Sonette Steczina, Saffie Mohran, Logan R.J. Bailey, Timothy S. McMillen, Kristina B. Kooiker, Neil B. Wood, Jennifer Davis, Michael J. Previs, Iacopo Olivotto, Jos è Manuel Pioner, Michael A. Geeves, Corrado Poggesi, Michael Regnier Source Type: research

MYBPC3-c.772G   >  a mutation results in haploinsufficiency and altered myosin cycling kinetics in a patient induced stem cell derived cardiomyocyte model of hypertrophic cardiomyopathy
Approximately 40% of hypertrophic cardiomyopathy mutations are linked to the sarcomere protein cardiac myosin binding protein-C (cMyBP-C). These mutations are either classified as missense mutations or truncation mutations. One mutation whose nature has been inconsistently reported in the literature is the MYBPC3-c.772G  > A mutation. Using patient-derived human induced pluripotent stem cells differentiated to cardiomyocytes (hiPSC-CMs), we have performed a mechanistic study of the structure-function relationship for this MYBPC3-c.772G > A mutation versus a mutation corrected, isogenic cell line. (Source: Journal o...
Source: Journal of Molecular and Cellular Cardiology - April 20, 2024 Category: Cytology Authors: Steczina Sonette, Saffie Mohran, Logan R.J. Bailey, Timothy S. McMillen, Kristina B. Kooiker, Neil B. Wood, Jennifer Davis, Michael J. Previs, Iacopo Olivotto, Jos è Manuel Pioner, Michael A. Geeves, Corrado Poggesi, Michael Regnier Source Type: research

Elucidating effects of the environmental pollutant benzo[a]pyrene [BaP] on cardiac arrhythmogenicity
Environmental pollution causes cardiovascular disease, heart failure, and arrythmias [1 –4]. Wildfire emissions are a complex mixture composed of particulate matter (PM), carbon monoxide, methane, nitrous oxide, and polyaromatic hydrocarbons, among others [5], which are linked to arrhythmias [6]. Benzo[a]pyrene is a polyaromatic hydrocarbon and known carcinogen in animal models and i s implicated in breast cancer, lung cancer, liver cancer, and skin cancer [7]. Therefore, the further impact of BaP on the cardiovascular system merits further investigation. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - April 20, 2024 Category: Cytology Authors: Johnson Y. Yang, Gema Mond éjar-Parreño, James W.S. Jahng, Yu Lu, Naomi Hamburg, Kari C. Nadeau, Daniel J. Conklin, Ronglih Liao, Mark Chandy, Joseph C. Wu Tags: Letter to the editor Source Type: research