Journal of Molecular and Cellular Cardiology This is an RSS file. You can use it to subscribe to this data in your favourite RSS reader or to display this data on your own website or blog.

Iron homeostasis in the heart: Molecular mechanisms and pharmacological implications
Iron is necessary for the life of practically all living things, yet it may also harm people toxically. Accordingly, humans and other mammals have evolved an effective and tightly regulatory system to maintain iron homeostasis in healthy tissues, including the heart. Iron deficiency is common in patients with heart failure, and is associated with worse prognosis in this population; while the prevalence of iron overload-related cardiovascular disorders is also increasing. Therefore, enhancing the therapy of patients with cardiovascular disorders requires a thorough understanding of iron homeostasis. (Source: Journal of Mole...
Source: Journal of Molecular and Cellular Cardiology - November 11, 2022 Category: Cytology Authors: Jiawei Zhang, Yijing Song, You Li, Han-Bin Lin, Xuexian Fang Tags: Review article Source Type: research

HuR-dependent expression of Wisp1 is necessary for TGF β-induced cardiac myofibroblast activity
Cardiac fibrosis is regulated by the activation and phenotypic switching of quiescent cardiac fibroblasts to active myofibroblasts, which have extracellular matrix (ECM) remodeling and contractile functions which play a central role in cardiac remodeling in response to injury. Here, we show that expression and activity of the RNA binding protein HuR is increased in cardiac fibroblasts upon transformation to an active myofibroblast. Pharmacological inhibition of HuR significantly blunts the TGF β-dependent increase in ECM remodeling genes, total collagen secretion, in vitro scratch closure, and collagen gel contraction in ...
Source: Journal of Molecular and Cellular Cardiology - November 10, 2022 Category: Cytology Authors: Lisa C. Green, Samuel Slone, Sarah R. Anthony, Adrienne R. Guarnieri, Sharon Parkins, Shannon M. Shearer, Michelle L. Nieman, Sudeshna Roy, Jeffrey Aube, Xiaoqing Wu, Liang Xu, Onur Kanisicak, Michael Tranter Source Type: research

Signaling network model of cardiomyocyte morphological changes in familial cardiomyopathy
Familial cardiomyopathy is a precursor of heart failure and sudden cardiac death. Over the past several decades, researchers have discovered numerous gene mutations primarily in sarcomeric and cytoskeletal proteins causing two different disease phenotypes: hypertrophic (HCM) and dilated (DCM) cardiomyopathies. However, molecular mechanisms linking genotype to phenotype remain unclear. Here, we employ a systems approach by integrating experimental findings from preclinical studies (e.g., murine data) into a cohesive signaling network to scrutinize genotype to phenotype mechanisms. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - November 10, 2022 Category: Cytology Authors: Ali Khalilimeybodi, Muhammad Riaz, Stuart G. Campbell, Jeffrey H. Omens, Andrew D. McCulloch, Yibing Qyang, Jeffrey J. Saucerman Source Type: research

An endogenous inhibitor of angiogenesis downregulated by hypoxia in human aortic valve stenosis promotes disease pathogenesis
Aortic valve stenosis is the most common valve disease in the western world. Central to the pathogenesis of this disease is the growth of new blood vessels (angiogenesis) within the aortic valve allowing infiltration of immune cells and development of intra-valve inflammation. Identifying the cellular mediators involved in this angiogenesis is important as this may reveal new therapeutic targets which could ultimately prevent the progression of aortic valve stenosis. Aortic valves from patients undergoing surgery for aortic valve replacement or dilation of the aortic arch were examined both ex vivo and in vitro. (Source: J...
Source: Journal of Molecular and Cellular Cardiology - November 3, 2022 Category: Cytology Authors: Christopher T.A. Lewis, Keith S. Mascall, Heather M. Wilson, Fiona Murray, Keith M. Kerr, George Gibson, Keith Buchan, Gary R. Small, Graeme F. Nixon Source Type: research

Generating robust human valvular interstitial cell cultures: Protocol and considerations
Research in heart valve biology is a growing field that has yet to elucidate the fundamentals of valve disease. Human valvular interstitial cells (hVICs) are the best option for studying the cellular mechanisms behind valvular pathologies. However, there is a wide range of isolation procedures for these cells published in the literature. To what extent various isolation methods, patient pathologies, and seeding densities influence the behaviour of hVICs remains unclear. Here, we present an optimised method of hVIC isolation from diseased human valves donated at the time of surgery. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - October 31, 2022 Category: Cytology Authors: Marcus Ground, Young Eun Park, Steve Waqanivavalagi, Karen Callon, Robert Walker, Paget Milsom, Jillian Cornish Source Type: research

Deletion of SIRT6 in vascular smooth muscle cells facilitates vascular calcification via suppression of DNA damage repair
Vascular calcification is an important risk factor for cardiovascular events, accompanied by DNA damage during the process. The sirtuin 6 (SIRT6) has been reported to alleviate atherosclerosis, which is related to the reduction of DNA damage. However, whether smooth muscle cell SIRT6 mediates vascular calcification involving DNA damage remains unclear. Western blot and immunofluorescence revealed that SIRT6 expression was decreased in human vascular smooth muscle cells (HVSMCs), human and mouse arteries during vascular calcification. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - October 28, 2022 Category: Cytology Authors: Siyi Wang, Li Li, Qingchun Liang, Yuanzhi Ye, Zirong Lan, Qianqian Dong, An Chen, Mingwei Fu, Yining Li, Xiaoyu Liu, Jing-Song Ou, Lihe Lu, Jianyun Yan Source Type: research

A transcriptomic atlas of drug-induced endothelial dysfunction in human endothelial cells
Drug-induced vascular burden is a critical challenge in both pharmaceutical development and clinical setting. In the past two decades, multiple drugs have been withdrawn from the market due to unanticipated adverse vascular complications, such as the increased risk of myocardial infarction and stroke (e.g., sibutramine and valdecoxib), heart valvular disease (e.g., pergolide and dexfenfluramine), and haemorrhagic stroke (e.g., phenylpropanolamine). Furthermore, many cancer drugs, such as anthracyclines, tyrosine kinase inhibitors (TKIs), and proteasome inhibitors, are also well-known to elicit a broad spectrum of vascular ...
Source: Journal of Molecular and Cellular Cardiology - October 27, 2022 Category: Cytology Authors: Chengyi Tu, Yu Liu, Damon R. Williams, Joseph C. Wu Tags: Letter to the Editor Source Type: research

Defective autophagy triggered by arterial cyclic stretch promotes neointimal hyperplasia in vein grafts via the p62/nrf2/slc7a11 signaling pathway
Autophagy is an adaptation mechanism to keep cellular homeostasis, and its deregulation is implicated in various cardiovascular diseases. After vein grafting, hemodynamic factors play crucial roles in neointimal hyperplasia, but the mechanisms are poorly understood. Here, we investigated the impacts of arterial cyclic stretch on autophagy of venous smooth muscle cells (SMCs) and its role in neointima formation after vein grafting. Rat jugular vein graft were generated via the ‘cuff’ technique. Autophagic flux in venous SMCs is impaired in 3-day, 1-week and 2-week grafted veins. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - October 26, 2022 Category: Cytology Authors: Yi Chen, Min Bao, Ji-Ting Liu, Han Bao, Shou-Min Zhang, Yue Lou, Ying-Xin Qi Source Type: research

Ferroptosis in heart failure
With its complicated pathobiology and pathophysiology, heart failure (HF) remains an increasingly prevalent epidemic that threatens global human health. Ferroptosis is a form of regulated cell death characterized by the iron-dependent lethal accumulation of lipid peroxides in the membrane system and is different from other types of cell death such as apoptosis and necrosis. Mounting evidence supports the claim that ferroptosis is mainly regulated by several biological pathways including iron handling, redox homeostasis, and lipid metabolism. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - October 20, 2022 Category: Cytology Authors: Xinquan Yang, Nicholas K. Kawasaki, Junxia Min, Takashi Matsui, Fudi Wang Tags: Review article Source Type: research

Early calcium and cardiac contraction defects in a model of phospholamban R9C mutation in zebrafish
The phospholamban mutation Arg 9 to Cys (R9C) has been found to cause a dilated cardiomyopathy in humans and in transgenic mice, with ventricular dilation and premature death. Emerging evidence suggests that phospholamban R9C is a loss-of-function mutation with dominant negative effect on SERCA2a activity. We imaged calcium and cardiac contraction simultaneously in 3 and 9  days-post-fertilization (dpf) zebrafish larvae expressing plnbR9C in the heart to unveil the early pathological pathway that triggers the disease. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - October 20, 2022 Category: Cytology Authors: Manuel Vicente, Jussep Salgado-Almario, Ariel A. Valiente-Gabioud, Michelle M. Collins, Pierre Vincent, Beatriz Domingo, Juan Llopis Source Type: research

Impaired CaV1.2 inactivation reduces the efficacy of calcium channel blockers in the treatment of LQT8
Mutations in the CaV1.2  L-type calcium channel can cause a profound form of long-QT syndrome known as long-QT type 8 (LQT8), which results in cardiac arrhythmias that are often fatal in early childhood. A growing number of such pathogenic mutations in CaV1.2 have been identified, increasing the need for targeted therapi es. As many of these mutations reduce channel inactivation; resulting in excess Ca2+ entry during the action potential, calcium channel blockers (CCBs) would seem to represent a promising treatment option. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - October 19, 2022 Category: Cytology Authors: Moradeke A. Bamgboye, Maria K. Traficante, Josiah Owoyemi, Deborah DiSilvestre, Daiana C.O. Vieira, Ivy E. Dick Source Type: research

Cyclophilin D knockout mice do not accumulate succinate during cardiac ischemia
A key driver of cardiac ischemia/reperfusion injury (IRI) and target for cardioprotection is the mitochondrial permeability transition pore (PTP). Persistent opening of the PTP leads to depolarization and increased permeability of the mitochondrial inner membrane followed by swelling and rupture, culminating in cell death [1]. The molecular characterization of the PTP remains contentious, however, cyclophilin D (CyD; a mitochondrial matrix peptidyl prolyl isomerase encoded by Ppif) is an important PTP modulator. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - October 6, 2022 Category: Cytology Authors: Hiran A. Prag, Duvaraka Kula-Alwar, Paolo Bernardi, Fabio Di Lisa, Michael P. Murphy, Thomas Krieg Tags: Letter to the editor Source Type: research

HFpEF etiology – Can focus on sex-specific mechanisms deliver insights for all?
In considering the heart failure with preserved ejection fraction (HFpEF) conundrum, the standard and disturbing preamble is almost ubiquitous: HFpEF has overtaken heart failure with reduced ejection fraction (HFrEF) as the major form of new failure diagnosis, incidence is escalating alarmingly, and there is no specific therapy for HFpEF. The historical perspective on the emergence of HFpEF has been elegantly chronicled [1]. It seems that achieving a definitive HFpEF diagnosis has always been problematic. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - September 29, 2022 Category: Cytology Authors: L.M.D. Delbridge, J.R. Bell, K.L. Weeks, A.J.A. Raaijmakers, K.M. Mellor Tags: Letter to the editor Source Type: research

Peli1 contributes to myocardial ischemia/reperfusion injury by impairing autophagy flux via its E3 ligase mediated ubiquitination of P62
Autophagy flux is impaired during myocardial ischemia/reperfusion (M-I/R) via the accumulation of autophagosome and insufficient clearance, which exacerbates cardiomyocyte death. Peli1 (Pellion1) is a RING finger domain-containing ubiquitin E3 ligase that could catalyze the polyubiquitination of substrate proteins. Peli1 has been demonstrated to play an important role in ischemic cardiac diseases. However, little is known about whether Peli1 is involved in the regulation of autophagy flux during M-I/R. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - September 27, 2022 Category: Cytology Authors: Jie Yang, Tingting Tong, Chenghao Zhu, Miao Zhou, Yuqing Jiang, Hao Chen, Linli Que, Li Liu, Guoqing Zhu, Tuanzhu Ha, Qi Chen, Chuanfu Li, Yong Xu, Jiantao Li, Yuehua Li Source Type: research

KMT2B-dependent RFK transcription activates the TNF- α/NOX2 pathway and enhances ferroptosis caused by myocardial ischemia-reperfusion
This study aims at exploring the role of KMT2B-mediated histone modification in MIRI. Peripheral blood samples were collected from 30 patients with acute myocardial infarction (AMI) and 30 healthy volunteers for analyses of the expression levels of KMT2B, riboflavin kinase (RFK), tumor necrosis factor (TNF)- α, and NADPH oxidase 2 (NOX2). (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - September 23, 2022 Category: Cytology Authors: Yuanyuan Cao, Fei Luo, Jia Peng, Zhenfei Fang, Qiming Liu, Shenghua Zhou Source Type: research