Increased α-Actinin-2 Expression in the Atrial Myocardium of Patients with Atrial Fibrillation Related to Rheumatic Heart Disease

Zhang, Lei; Zhang, Nan; Tang, Xue; Liu, Fa-jin; Luo, Suxin

doi:10.1159/000446362

Cited by 17 publications

(14 citation statements)

References 35 publications

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“…Finally, we would like to clarify that our hypothesis is based on data of patients without rheumatic heart disease. However, patients with IAB and rheumatic disease probably have an even higher risk of stroke as the burden of atrial fibrosis is noteworthy in patients with AF and rheumatic heart disease [ 27 ].…”

Section: Should Anticoagulation Be Used In Some Patients With Advancementioning

confidence: 99%

Surface ECG interatrial block-guided treatment for stroke prevention: rationale for an attractive hypothesis

Luna

Martínez‐Sellés

Bayés‐Genís

et al. 2017

BMC Cardiovasc Disord

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Atrial fibrillation (AF) is the most common sustained arrhythmia and is associated with stroke, cognitive impairment, and cardiovascular death. Some predisposing factors − as aging, diabetes, hypertension − induce and maintain electrophysiological and ultrastructural remodeling that usually includes fibrosis. Interatrial conduction disturbances play a crucial role in the initiation of atrial fibrosis and in its associated complications. The diagnosis of interatrial blocks (IABs) is easy to perform using the surface ECG. IAB is classified as partial when the P wave duration is ≥120 ms, and advanced if the P wave also presents a biphasic pattern in II, III and aVF. IAB is very frequent in the elderly and, particularly in the case of the advanced type, is associated with AF, AF recurrences, stroke, and dementia. The anticoagulation in elderly patients at high risk of AF without documented arrhythmias is an open issue but recent data suggest that it might have a role, particularly in elderly patients with structural heart disease, high CHA2DS2VASc (Congestive heart failure/left ventricular dysfunction, Hypertension, Age ≥ 75 [doubled], Diabetes, Stroke [doubled] – Vascular disease, Age 65–74, and Sex category [female]), and advanced IAB. In this debate, we discuss the association of surface ECG IAB, a marker of atrial fibrosis, with AF and stroke. We also present the rationale that justifies further studies regarding anticoagulation in some of these patients.

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Section: Should Anticoagulation Be Used In Some Patients With Advancementioning

confidence: 99%

Surface ECG interatrial block-guided treatment for stroke prevention: rationale for an attractive hypothesis

Luna

Martínez‐Sellés

Bayés‐Genís

et al. 2017

BMC Cardiovasc Disord

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“…At present, there are few studies on the signaling pathways related to the pathogenesis of RHD, and there are only 6 signaling pathways with signi cant research progress: RhoA/Rho-dependent kinase (RhoA/ROCK) signaling pathway,Mitogen-activated protein kinase (MAPK) signaling pathway Protein kinase B/S6 kinase (AKT/S6K) signaling pathway TGF-β1/Smad signaling pathway Wnt signaling pathway and S1PR1/STAT3 signaling pathway [34,[51][52][53][54][55]. And there are only three potential intervention targets found in these signaling pathway studies: Intervene in the expression of interferon (IFN)-γ and tumour necrosis factor (TNF)-α to regulate extracellular matrix remodeling to reduce heart damage caused by RHD; Intervene in AKT/S6K signaling pathway to inhibit TGF-β1-induced broblasts; Intervene in the S1PR1/STAT3 signaling pathway to reduce RHDinduced valvular damage.…”

Section: Discussionmentioning

confidence: 99%

Intervening in the S1PR1/STAT3 Signaling Pathway Attenuates Valvular Damage Due to Rheumatic Heart Disease

Xian

Chen

et al. 2020

Preprint

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Background: Rheumatic heart disease (RHD) affects many patients every year, but its pathogenesis is still unclear. Recent studies have found that the sphingosine 1-phosphate receptor 1 (S1PR1)/signal transducer and activator of transcription 3 (STAT3) signaling pathway is involved in valvular damage by promoting the differentiation of T helper 17 (Th17) cells during the development of valvular damage caused by RHD. In this work, we investigated whether altering the S1PR1/STAT3 signaling pathway attenuates valvular damage due to RHD. Methods: Inactivated Group A streptococci (GAS) was used to establish the RHD rat model. Recombinant adeno-associated virus (serotype 9) vectors carrying the S1PR1 overexpression sequence was used to overexpress the expression of S1PR1. STAT3-small interfering RNA (STAT3-siRNA) was used to inhibit the expression of STAT3. Reverse transcription-quantitative PCR (RT-qPCR) was used to detect the mRNA expression of S1PR1, STAT3, collagen type III α1 chain (Col3a1) and fibroblast-specific protein 1 (FSP1). Western blotting (WB) and immunohistochemistry were used to detect the protein expression of S1PR1, STAT3, phosphorylated (p-) STAT3, retinoic acid-related orphan receptor gamma T (RORγt). Enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry were used to detect the levels of interleukin (IL)-6 and IL-17. Haematoxylin and eosin (H&E) staining and Sirius red staining were used to evaluate the degree of inflammation and fibrosis in valve tissues.Results: The expression of S1PR1 in valve tissues of RHD model rats was decreased. The levels of IL-6 and IL-17 in valves and serum of RHD model rats were increased as well as an increase of p-STAT3. The degree of valvular inflammation and fibrosis of RHD model rats was increased. Overexpression of S1PR1 and Inhibition of STAT3 overexpressed S1PR1 expression and decreased STAT3 expression respectively and reduced the total amount of p-STAT3, resulting in decreased expression of IL-6, IL-17 and RORγt and reduced the degree of valvular inflammatory and fibrosis. Conclusions: These results suggest that the S1PR1/STAT3 signaling pathway is involved in regulating the Th17 cell-related cytokines during the vavular damage due to RHD, and altering the S1PR1/STAT3 signaling pathway could affect the expression of Th17 cell-related cytokines then attenuate the vavular damage due to RHD.

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“…TGF-β1/Smad signalling pathway and RHD. Zhang et al (23) also found that the TGF-β1/Smad signalling pathway increased the expression of α-actinin-2 and participated in the process of RHD-induced atrial fibrosis. Patients with RHD-induced AF were used as the experimental group and patients with congenital heart disease and SR who underwent heart surgery were used as controls.…”

Section: Signalling Pathways Implicated In the Pathogenesis Of Rheumamentioning

confidence: 97%

Signalling pathways implicated in the pathogenesis of rheumatic heart disease (Review)

Xian

Zeng

2020

Exp Ther Med

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Rheumatic heart disease (RHD) is frequently encountered in underdeveloped areas and primarily affects patients under the age of 40 years old. The pathogenesis of RHD has yet to be fully elucidated and surgical treatment remains the only option, which is expensive and technically demanding for patients in less developed areas. Signalling pathways are crucial for the occurrence and development of several diseases, and researchers worldwide have made progress in elucidating the signalling pathways associated with the pathogenesis of RHD. The aim of the present review was to discuss 6 signalling pathways implicated in the pathogenesis of RHD, summarize the methods and progress of these studies and propose future research directions. Important information on the pathogenesis of RHD according to the current progress of signalling pathway studies was also summarized, in the hope that this review may serve as a reference for future research on the signalling pathways involved in the pathogenesis of RHD.

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Increased α-Actinin-2 Expression in the Atrial Myocardium of Patients with Atrial Fibrillation Related to Rheumatic Heart Disease

Cited by 17 publications

References 35 publications

Surface ECG interatrial block-guided treatment for stroke prevention: rationale for an attractive hypothesis

Surface ECG interatrial block-guided treatment for stroke prevention: rationale for an attractive hypothesis

Intervening in the S1PR1/STAT3 Signaling Pathway Attenuates Valvular Damage Due to Rheumatic Heart Disease

Signalling pathways implicated in the pathogenesis of rheumatic heart disease (Review)

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