MiR-324-3p Regulates Fibroblast Proliferation via Targeting TGF-β1 in Atrial Fibrillation

Xu, Jiali; Lei, Sisi; Sun, Shuhong; Zhang, Wei; Zhu, Feiqi; Yang, Hsiu‐Chiung; Xu, Qingmei; Zhang, Bing; Li, Hui; Zhu, Mingli; Hu, Xiaotao; Zhang, Heng; Tang, Bi; Kang, Pan

doi:10.1536/ihj.20-423

Cited by 11 publications

(6 citation statements)

References 38 publications

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“…Exosome cargo selectively includes a large array of distinct biologically active molecules, such as lipids, proteins, coding and non-coding RNAs (microRNAs, lncRNAs and circR-NAs) [1][2][3]. Evidence of the differential and selective distribution of combinations of these molecules, derived from distinct cardiovascular cell sources, i.e., cardiomyocytes, endothelial and/or epicardial cells and infiltrated immune cells, has been largely documented [298][299][300][301][302][303][304][305]. Such differential distribution, particularly of microRNAs, lncRNAs and circRNAs, in distinct pathological conditions has provided molecular hallmarks that can be exploited as sensitive biomarkers for the early diagnosis and prediction of distinct cardiovascular pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

“…Different molecular cascades have been implicated as triggering factors of AF. In this context, the contribution of small EVs to AF has been reported to play a fundamental role in inducing fibrosis [298][299][300][301][302], inflammation [302][303][304][305], oxidative stress [302] and apoptosis [306]. Within the context of AF-atrial fibrosis, both microRNAs and lncRNAs have been identified.…”

Section: Mechanistic Insights Into Small Extracellular Vesicle Relate...mentioning

confidence: 99%

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Unraveling the Signaling Dynamics of Small Extracellular Vesicles in Cardiac Diseases

Caño-Carrillo,

Castillo-Casas,

Franco

et al. 2024

Cells

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Effective intercellular communication is essential for cellular and tissue balance maintenance and response to challenges. Cellular communication methods involve direct cell contact or the release of biological molecules to cover short and long distances. However, a recent discovery in this communication network is the involvement of extracellular vesicles that host biological contents such as proteins, nucleic acids, and lipids, influencing neighboring cells. These extracellular vesicles are found in body fluids; thus, they are considered as potential disease biomarkers. Cardiovascular diseases are significant contributors to global morbidity and mortality, encompassing conditions such as ischemic heart disease, cardiomyopathies, electrical heart diseases, and heart failure. Recent studies reveal the release of extracellular vesicles by cardiovascular cells, influencing normal cardiac function and structure. However, under pathological conditions, extracellular vesicles composition changes, contributing to the development of cardiovascular diseases. Investigating the loading of molecular cargo in these extracellular vesicles is essential for understanding their role in disease development. This review consolidates the latest insights into the role of extracellular vesicles in diagnosis and prognosis of cardiovascular diseases, exploring the potential applications of extracellular vesicles in personalized therapies, shedding light on the evolving landscape of cardiovascular medicine.

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Section: Discussionmentioning

confidence: 99%

Section: Mechanistic Insights Into Small Extracellular Vesicle Relate...mentioning

confidence: 99%

Unraveling the Signaling Dynamics of Small Extracellular Vesicles in Cardiac Diseases

Caño-Carrillo,

Castillo-Casas,

Franco

et al. 2024

Cells

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“…MiR-324-3p has been disclosed to be involved in many diseases progression. For example, miR-324-3p targets TGF-β1 to modulate fibroblast proliferation in atrial fibrillation [ 42 ]. In addition, miR-324-3p targets WNT2B to retard nasopharyngeal carcinoma progression [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine improves oxygen-glucose deprivation/reoxygenation (OGD/R) -induced neurological injury through regulating SNHG11/miR-324-3p/VEGFA axis

Chen

Fan

2021

Bioengineered

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Dexmedetomidine (Dex) has been reported to exhibit neuroprotective effects through various regulatory mechanisms. This study aims to investigate the role and molecular mechanism of SNHG11 in Dex-mediated neuroprotection. The ischemic stroke (IS) model was established in vivo by middle cerebral artery occlusion (MCAO) and in vitro by oxygen-glucose deprivation and reperfusion (OGD/R)-treated SH-SY5Y. SNHG11 was highly expressed after OGD/R, and Dex improved OGD/R-induced neurological injury. Additionally, Dex reversed the effects of SNHG11 on OGD/R-induced neurological injury. Furthermore, we found that SNHG11 upregulated vascular endothelial growth factor A (VEGFA) expression by targeting miR-324-3p. Through rescue assays, it was confirmed that SNHG11 regulated OGD/R-induced neurological injury through increasing VEGFA expression. At last, Dex was also discovered to improve neurological injury through regulating SNHG11 in the rat model. In conclusion, our work demonstrated that Dex improved OGD/R-induced neurological injury via SNHG11/miR-324-3p/VEGFA axis. These findings may offer a novel therapeutic strategy for IS treatment.

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“…TGF-β signaling is strongly associated with these structural changes [ 44 ]. Various microRNAs and long noncoding RNAs seem to regulate cardiac fibroblast profibrogenic activity [ 45 , 46 , 47 , 48 , 49 ]. A recently discovered crosstalk between Slit2-Robo1 and TGF-β1/Smad pathways promises potential therapeutic targets against atrial fibrosis [ 50 ].…”

Section: Atrial Fibrillation Pathogenesismentioning

confidence: 99%

Molecular Insights in Atrial Fibrillation Pathogenesis and Therapeutics: A Narrative Review

et al. 2021

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The prevalence of atrial fibrillation (AF) is bound to increase globally in the following years, affecting the quality of life of millions of people, increasing mortality and morbidity, and beleaguering health care systems. Increasingly effective therapeutic options against AF are the constantly evolving electroanatomic substrate mapping systems of the left atrium (LA) and ablation catheter technologies. Yet, a prerequisite for better long-term success rates is the understanding of AF pathogenesis and maintenance. LA electrical and anatomical remodeling remains in the epicenter of current research for novel diagnostic and treatment modalities. On a molecular level, electrical remodeling lies on impaired calcium handling, enhanced inwardly rectifying potassium currents, and gap junction perturbations. In addition, a wide array of profibrotic stimuli activates fibroblast to an increased extracellular matrix turnover via various intermediaries. Concomitant dysregulation of the autonomic nervous system and the humoral function of increased epicardial adipose tissue (EAT) are established mediators in the pathophysiology of AF. Local atrial lymphomononuclear cells infiltrate and increased inflammasome activity accelerate and perpetuate arrhythmia substrate. Finally, impaired intracellular protein metabolism, excessive oxidative stress, and mitochondrial dysfunction deplete atrial cardiomyocyte ATP and promote arrhythmogenesis. These overlapping cellular and molecular alterations hinder us from distinguishing the cause from the effect in AF pathogenesis. Yet, a plethora of therapeutic modalities target these molecular perturbations and hold promise in combating the AF burden. Namely, atrial selective ion channel inhibitors, AF gene therapy, anti-fibrotic agents, AF drug repurposing, immunomodulators, and indirect cardiac neuromodulation are discussed here.

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MiR-324-3p Regulates Fibroblast Proliferation via Targeting TGF-β1 in Atrial Fibrillation

Cited by 11 publications

References 38 publications

Unraveling the Signaling Dynamics of Small Extracellular Vesicles in Cardiac Diseases

Unraveling the Signaling Dynamics of Small Extracellular Vesicles in Cardiac Diseases

Dexmedetomidine improves oxygen-glucose deprivation/reoxygenation (OGD/R) -induced neurological injury through regulating SNHG11/miR-324-3p/VEGFA axis

Molecular Insights in Atrial Fibrillation Pathogenesis and Therapeutics: A Narrative Review

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