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.

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

AICAR confers prophylactic cardioprotection in doxorubicin-induced heart failure in rats
Doxorubicin (DOX) is a widely used chemotherapeutic agent that can cause serious cardiotoxic side effects, leading to heart failure (HF). Impaired mitochondrial function is thought to be key factor driving progression into HF. We have previously shown in a rat model of DOX-HF that heart failure with reduced ejection fraction correlates with mitochondrial loss and dysfunction. Adenosine monophosphate-dependent kinase (AMPK) is a cellular energy sensor, regulating mitochondrial biogenesis and energy metabolism, including fatty acid oxidation. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - April 19, 2024 Category: Cytology Authors: Anurag Choksey, Ryan D. Carter, Benjamin D. Thackray, Vicky Ball, Brett W.C. Kennedy, Lea Hong Tuan Ha, Eshita Sharma, John Broxholme, Marcos Castro-Guarda, Michael P. Murphy, Lisa C. Heather, Damian J. Tyler, Kerstin N. Timm Source Type: research

An update on the mechanisms of Takotsubo syndrome: “At the end an acute coronary syndrome”
Takotsubo syndrome (TTS) is an acute reversible form of myocardial dysfunction, often preceded by a physical or emotional stressful event, that acts as a trigger. Despite, recent advances in the comprehension of the mechanisms leading to TTS, its pathophysiology is far from being completely understood. However, several studies seem to suggest that an acute coronary microvascular dysfunction may represent a crucial pathogenic mechanism involved in TTS occurrence.In this article, we aim to review the complex pathophysiology of TTS and the possible different mechanisms underlying this clinical condition, focusing on the role ...
Source: Journal of Molecular and Cellular Cardiology - April 17, 2024 Category: Cytology Authors: Filippo Crea, Giulia Iannaccone, Giulia La Vecchia, Rocco A. Montone Tags: Review article Source Type: research

Differential bioenergetics in adult rodent cardiomyocytes isolated from the right versus left ventricle
The heart is a highly metabolically active organ with ∼90% of its ATP production derived from mitochondrial oxidative phosphorylation. Mitochondrial dysfunction associated with the bioenergetic collapse seen in left ventricular (LV) heart failure is characterized by depressed oxidative phosphorylation, a switch away from fatty acid oxidation, and alt ered mitochondrial dynamics. Accumulating evidence suggests that mitochondrial mechanisms underlying right ventricular (RV) failure may diverge from those of LV failure [1], underscoring the need for comparative study of RV versus LV. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - April 11, 2024 Category: Cytology Authors: Quyen L. Nguyen, Krithika Rao, John C. Sembrat, Claudette St. Croix, Brett A. Kaufman, Iain Scott, Eric Goetzman, Sruti Shiva Tags: Letter to the editor Source Type: research

Triiodothyronine induces a proinflammatory monocyte/macrophage profile and impedes cardiac regeneration
Neonatal mouse hearts can regenerate post-injury, unlike adult hearts that form fibrotic scars. The mechanism of thyroid hormone signaling in cardiac regeneration warrants further study. We found that triiodothyronine impairs cardiomyocyte proliferation and heart regeneration in neonatal mice after apical resection. Single-cell RNA-Sequencing on cardiac CD45-positive leukocytes revealed a pro-inflammatory phenotype in monocytes/macrophages after triiodothyronine treatment. Furthermore, we observed that cardiomyocyte proliferation was inhibited by medium from triiodothyronine-treated macrophages, while triiodothyronine itse...
Source: Journal of Molecular and Cellular Cardiology - April 10, 2024 Category: Cytology Authors: Ziwei Chen, Dongcheng Cai, Yifan Xie, Jiajun Zhong, Mengge Wu, Huijun Yang, Jie Feng, Hong Lian, Kefei Dou, Yu Nie Source Type: research

Unraveling the Gordian knot of coronary pressure-flow autoregulation
The coronary circulation has the inherent ability to maintain myocardial perfusion constant over a wide range of perfusion pressures. The phenomenon of pressure-flow autoregulation is crucial in response to flow-limiting atherosclerotic lesions which diminish coronary driving pressure and increase risk of myocardial ischemia and infarction. Despite well over half a century of devoted research, understanding of the mechanisms responsible for autoregulation remains one of the most fundamental and contested questions in the field today. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - April 10, 2024 Category: Cytology Authors: Johnathan D. Tune, Cooper M. Warne, Salman I. Essajee, Selina M. Tucker, C. Alberto Figueroa, Gregory M. Dick, Daniel A. Beard Tags: Review article Source Type: research

Titin's cardiac-specific N2B element is critical to mechanotransduction during volume overload of the heart
In this study, we focused on investigating the role of the cardiac-specific N2B element within the spring region of titin, which has been proposed to function as a mechanosensor. To assess its significance, we conducted experiments using N2B knockout (KO) mice and wildtype (WT) mice, subjecting them to three different conditions: 1) cardiac pressure overload induced by transverse aortic constriction (TAC), 2) volume overload caused by aortocaval fistula (ACF), and 3) exercise-induced hypertrophy through swimming. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - April 9, 2024 Category: Cytology Authors: Joshua Strom, Mathew Bull, Jochen Gohlke, Chandra Saripalli, Mei Methawasin, Michael Gotthardt, Henk Granzier Source Type: research

Essential role of Alix in regulating cardiomyocyte exosome biogenesis under physiological and stress conditions
Exosomes released by cardiomyocytes are essential mediators of intercellular communications within the heart, and various exosomal proteins and miRNAs are associated with cardiovascular diseases. However, whether the endosomal sorting complex required for transport (ESCRT) and its key component Alix is required for exosome biogenesis within cardiomyocyte remains poorly understood. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - April 8, 2024 Category: Cytology Authors: Xinjian Wang, Shuxian Han, Jinxiu Liang, Chen Xu, Ranran Cao, Shuoyang Liu, Yi Luan, Ying Gu, Peidong Han Source Type: research

Does female sex matter in a chronic intermittent hypoxia mouse model?
Intermittent hypoxia (IH) occurs in patients with obstructive sleep apnea, where periods of hypoxia alternate with periods of normoxia, leading to cardiovascular damage [1]. Indeed, IH induces oxidative stress and systemic inflammation through the activation of hypoxia inducible factor 1 subunit alpha (HIF α), nuclear factor kappa-B (NFκB) and toll like receptor 4 (TLR4), which contribute to accelerated atherosclerosis development [2]. To study the development of atherosclerotic lesions under chronic intermittent hypoxia (CIH) in vivo, the majority of researchers have used a male ApoE−/− mouse m odel. (Source: Journa...
Source: Journal of Molecular and Cellular Cardiology - April 5, 2024 Category: Cytology Authors: N. Kindt, K. Thayse, N. Dalil, A. Trelcat, S. Carlier Tags: Letter to the editor Source Type: research

Deficiency of smooth muscle cell ILF3 alleviates intimal hyperplasia via HMGB1 mRNA degradation-mediated regulation of the STAT3/DUSP16 axis
Intimal hyperplasia is a complicated pathophysiological phenomenon attributable to in-stent restenosis, and the underlying mechanism remains unclear. Interleukin enhancer-binding factor 3 (ILF3), a double-stranded RNA-binding protein involved in regulating mRNA stability, has been recently demonstrated to assume a crucial role in cardiovascular disease; nevertheless, its impact on intimal hyperplasia remains unknown. In current study, we used samples of human restenotic arteries and rodent models of intimal hyperplasia, we found that vascular smooth muscle cell (VSMC) ILF3 expression was markedly elevated in human restenot...
Source: Journal of Molecular and Cellular Cardiology - April 5, 2024 Category: Cytology Authors: Ya-min Hou, Bo-han Xu, Qiu-ting Zhang, Jie Cheng, Xu Zhang, Hong-rui Yang, Ze-ying Wang, Peng Wang, Ming-xiang Zhang Source Type: research

Corrigendum to “Cholesterol-induced HRD1 reduction accelerates vascular smooth muscle cell senescence via stimulation of endoplasmic reticulum stress-induced reactive oxygen species” [Journal of Molecular and Cellular Cardiology 187(2024) 51–64]
The authors regret (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - April 4, 2024 Category: Cytology Authors: Linli Wang, Min Wang, Haiming Niu, Yaping Zhi, Shasha Li, Xuemin He, Zhitao Ren, Shiyi Wen, Lin Wu, Siying Wen, Rui Zhang, Zheyao Wen, Jing Yang, Ximei Zhang, Yanming Chen, Xiaoxian Qian, Guojun Shi Tags: Corrigendum Source Type: research

C166 EVs potentiate miR cardiac reprogramming via miR-148a-3p
We have demonstrated that directly reprogramming cardiac fibroblasts into new cardiomyocytes via miR combo improves cardiac function in the infarcted heart. However, major challenges exist with delivery and efficacy. During a screening based approach to improve delivery, we discovered that C166-derived EVs were effective delivery agents for miR combo both in vitro and in vivo. In the latter, EV mediated delivery of miR combo induced significant conversion of cardiac fibroblasts into cardiomyocytes (~20%), reduced fibrosis and improved cardiac function in a myocardial infarction injury model. (Source: Journal of Molecular a...
Source: Journal of Molecular and Cellular Cardiology - April 4, 2024 Category: Cytology Authors: Hualing Sun, Xinghua Wang, Richard E. Pratt, Victor J. Dzau, Conrad P. Hodgkinson Source Type: research

Reduced cardiac antioxidant defenses mediate increased susceptibility to workload-induced myocardial injury in males with genetic cardiomyopathy
Ongoing cardiomyocyte injury is a major mechanism in the progression of heart failure, particularly in dystrophic hearts. Due to the poor regenerative capacity of the adult heart, cardiomyocyte death results in the permanent loss of functional myocardium. Understanding the factors contributing to myocyte injury is essential for the development of effective heart failure therapies. As a model of persistent cardiac injury, we examined mice lacking β-sarcoglycan (β-SG), a key component of the dystrophin glycoprotein complex (DGC). (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - March 23, 2024 Category: Cytology Authors: Tatyana A. Vetter, Preethy Parthiban, Jackie A. Stevens, Xavier S. Revelo, Mark J. Kohr, DeWayne Townsend Source Type: research

Atrial proteomic profiling reveals a switch towards profibrotic gene expression program in CREM-Ib ΔC-X mice with persistent atrial fibrillation
Overexpression of the CREM (cAMP response element-binding modulator) isoform CREM-Ib ΔC-X in transgenic mice (CREM-Tg) causes the age-dependent development of spontaneous AF. (Source: Journal of Molecular and Cellular Cardiology)
Source: Journal of Molecular and Cellular Cardiology - March 19, 2024 Category: Cytology Authors: Shuai Zhao, Mohit M. Hulsurkar, Satadru K. Lahiri, Yuriana Aguilar-Sanchez, Elda Munivez, Frank Ulrich M üller, Antrix Jain, Anna Malovannaya, Kendrick Yiu, Svetlana Reilly, Xander H.T. Wehrens Source Type: research