Corrigendum to: Uncovering the skeleton in the heart: an unusual case of mitral annular calcification extending to the left ventricular myocardium

Abstract Background To investigate the effects of telmisartan on the protein profiles of the left ventricular myocardium in spontaneously hypertensive rats (SHR). Methods Sixteen SHR were randomly divided into control and telmisartan treatment groups. Rats were treated with sterile water (10 ml/kg) or telmisartan (4.33 mg/kg) by gavage for 12 weeks. Wistar-Kyoto (WKY) rats treated with sterile water (10 ml/kg) as controls. At the end of 12 weeks of control or telmisartan treatment, rats were sacrificed, and hearts were collected for protein preparations, isotope labeling, and mass spectrometric analysis. Results In total, there were 23 differentially expressed proteins in the left ventricular myocardium between control and telmisartan treatment groups in SHR. Compared with the telmisartan group, the upregulated proteins in the SHR were dual-specificity mitogen-activated protein kinase kinase 3-like, transgelin, and haptoglobin subtype 2. The downregulated proteins in the SHR were as follows: von Willebrand factor (fragment), kininogen 1, small ribonucleoprotein-related protein, fibrinogen beta chain, protein mass 3 (fragment), proteasome 26s, heat shock protein 27-related protein 1, tenascin X, fibronectin subtype 2, transferrin receptor protein, platelets 1, cathepsin L1, complement factor B, isoform CRA_b, fibrinogen isomer, immunoglobulin heavy chain (γ polypeptide), and α 1 antiprotease. Conclusions Telmisartan differentially regulates myocardial protein expression in hypertensive rats including heat shock protein 27, fibrinogen, fibronectin, proteasome 26s and transgelin, as well as proteins in biochemical, metabolic, and signal transduction pathways. These changes in protein expression may contribute to the antihypertrophic effects of telmisartan in hypertension.

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Remodeling of t-system and proteins underlying excitation-contraction coupling in aging versus failing human heart

npj Aging and Mechanisms of Disease ◽

10.1038/s41514-021-00066-7 ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Yankun Lyu ◽

Vipin K. Verma ◽

Younjee Lee ◽

Iosif Taleb ◽

Rachit Badolia ◽

...

Keyword(s):

Heart Function ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Left Ventricular Myocardium ◽

Excitation Contraction Coupling ◽

Transverse Tubular System ◽

Contraction Coupling ◽

Senescent Phenotype ◽

Cellular Microstructure ◽

T System

AbstractIt is well established that the aging heart progressively remodels towards a senescent phenotype, but alterations of cellular microstructure and their differences to chronic heart failure (HF) associated remodeling remain ill-defined. Here, we show that the transverse tubular system (t-system) and proteins underlying excitation-contraction coupling in cardiomyocytes are characteristically remodeled with age. We shed light on mechanisms of this remodeling and identified similarities and differences to chronic HF. Using left ventricular myocardium from donors and HF patients with ages between 19 and 75 years, we established a library of 3D reconstructions of the t-system as well as ryanodine receptor (RyR) and junctophilin 2 (JPH2) clusters. Aging was characterized by t-system alterations and sarcolemmal dissociation of RyR clusters. This remodeling was less pronounced than in HF and accompanied by major alterations of JPH2 arrangement. Our study indicates that targeting sarcolemmal association of JPH2 might ameliorate age-associated deficiencies of heart function.

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Myxomatous Mitral Valve Disease with Mitral Valve Prolapse and Mitral Annular Disjunction: Clinical and Functional Significance of the Coincidence

Journal of Cardiovascular Development and Disease ◽

10.3390/jcdd8020009 ◽

2021 ◽

Vol 8 (2) ◽

pp. 9

Author(s):

Nina C. Wunderlich ◽

Siew Yen Ho ◽

Nir Flint ◽

Robert J. Siegel

Keyword(s):

Mitral Valve ◽

Mitral Valve Disease ◽

Morphological Changes ◽

Morphological Characteristics ◽

Mitral Annulus ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Valve Disease ◽

Left Ventricular Myocardium ◽

Basal Portion

The morphological changes that occur in myxomatous mitral valve disease (MMVD) involve various components, ultimately leading to the impairment of mitral valve (MV) function. In this context, intrinsic mitral annular abnormalities are increasingly recognized, such as a mitral annular disjunction (MAD), a specific anatomical abnormality whereby there is a distinct separation between the mitral annulus and the left atrial wall and the basal portion of the posterolateral left ventricular myocardium. In recent years, several studies have suggested that MAD contributes to myxomatous degeneration of the mitral leaflets, and there is growing evidence that MAD is associated with ventricular arrhythmias and sudden cardiac death. In this review, the morphological characteristics of MAD and imaging tools for diagnosis will be described, and the clinical and functional aspects of the coincidence of MAD and myxomatous MVP will be discussed.

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β-blockade abolishes the augmented cardiac tPA release induced by transactivation of heterodimerised bradykinin receptor-2 and β2-adrenergic receptor in vivo

Thrombosis and Haemostasis ◽

10.1160/th14-01-0059 ◽

2014 ◽

Vol 112 (11) ◽

pp. 951-959 ◽

Cited By ~ 1

Author(s):

Morten Eriksen ◽

Arnfinn Ilebekk ◽

Alessandro Cataliotti ◽

Cathrine Rein Carlson ◽

Torstein Lyberg ◽

...

Keyword(s):

Adrenergic Receptor ◽

Sympathetic Nerves ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Left Ventricular Myocardium ◽

Adrenergic Stimulation ◽

Β2 Adrenergic Receptor ◽

Β Blocker

SummaryBradykinin (BK) receptor-2 (B2R) and β2-adrenergic receptor (β2AR) have been shown to form heterodimers in vitro. However, in vivo proofs of the functional effects of B2R-β2AR heterodimerisation are missing. Both BK and adrenergic stimulation are known inducers of tPA release. Our goal was to demonstrate the existence of B2R-β2AR heterodimerisation in myocardium and to define its functional effect on cardiac release of tPA in vivo. We further investigated the effects of a non-selective β-blocker on this receptor interplay. To investigate functional effects of B2R-β2AR heterodimerisation (i. e. BK transactivation of β2AR) in vivo, we induced serial electrical stimulation of cardiac sympathetic nerves (SS) in normal pigs that underwent concomitant BK infusion. Both SS and BK alone induced increases in cardiac tPA release. Importantly, despite B2R desensitisation, simultaneous BK infusion and SS (BK+SS) was characterised by 2.3 ± 0.3-fold enhanced tPA release compared to SS alone. When β-blockade (propranolol) was introduced prior to BK+SS, tPA release was inhibited. A persistent B2R-β2AR heterodimer was confirmed in BK-stimulated and nonstimulated left ventricular myocardium by immunoprecipitation studies and under non-reducing gel conditions. All together, these results strongly suggest BK transactivation of β2AR leading to enhanced β2AR-mediated release of tPA. Importantly, non-selective β-blockade inhibits both SS-induced release of tPA and the functional effects of B2R-β2AR heterodimerisation in vivo, which may have important clinical implications.

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Heart transplantation in an adult patient with isolated noncompaction of the left ventricular myocardium

Medicina ◽

10.3390/medicina46030027 ◽

2010 ◽

Vol 46 (3) ◽

pp. 193 ◽

Cited By ~ 6

Author(s):

Sigita Glaveckaitė ◽

Kęstutis Ručinskas ◽

Jelena Čelutkienė ◽

Vytė Maneikienė ◽

Diana Zakarkaitė ◽

...

Keyword(s):

Heart Transplantation ◽

Adult Patient ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Left Ventricular Myocardium ◽

Important Process ◽

Ventricular Noncompaction ◽

Myocardial Development ◽

Myocardial Fibers ◽

Heart Lesions

Isolated noncompaction of the ventricular myocardium is defined as a rare cardiomyopathy caused by intrauterine arrest of compaction of the myocardial fibers and meshwork, an important process in myocardial development, in absence of any coexisting congenital heart lesions. A lot of controversies exist about diagnostic criteria, nomenclature, origin, pathogenesis, and prognosis of this disease. Here, we describe an adult patient with isolated left ventricular noncompaction who presented with worsening congestive heart failure and was successfully treated with heart transplantation.

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