miR-133: A Suppressor of Cardiac Remodeling?

Frontiers in Pharmacology, Journal Year: 2018, Volume and Issue: 9

Published: Aug. 17, 2018

Cardiac remodeling, characterized by mechanical remodeling and electrical is a significant pathophysiological process involved in almost all forms of heart diseases. MicroRNAs (miRNAs) are group 20-25 nt non-coding RNAs, which regulate gene expression primarily through mRNA degradation or post-transcriptional repression sequence-specific manner. In the human genome, there three known miR-133 genes: miR-133a-1, miR-133a-2 miR-133b found on chromosomes 18, 20 6 respectively, mainly expressed muscle tissue appear to repress non-muscle genes. Increasing evidence indicates that participates proliferation, differentiation, survival, hypertrophic growth conduction cardiac cells, essential for fibrosis, hypertrophy arrhythmia. Nevertheless, roles ambiguous mechanisms also sophisticated, involving many target genes signaling pathways, such as Rhoa, MAPK,TGFβ/Smad, PI3K/Akt, etc. Therefore, this review, we summarize critical potential remodeling.

Language: Английский

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Circular noncoding RNAs as potential therapies and circulating biomarkers for cardiovascular diseases

Acta Pharmacologica Sinica, Journal Year: 2018, Volume and Issue: 39(7), P. 1100 - 1109

Published: March 22, 2018

Language: Английский

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NLRP3-mediated pyroptosis aggravates pressure overload-induced cardiac hypertrophy, fibrosis, and dysfunction in mice: cardioprotective role of irisin

Cell Death Discovery, Journal Year: 2021, Volume and Issue: 7(1)

Published: March 15, 2021

Abstract The exact mechanism of myocardial hypertrophy has not been completely elucidated. NOD-like receptor protein 3 (NLRP3) and the pyroptotic cascade play a critical role in cardiac inflammation. myokine irisin can inhibit NLRP3 activation, although its action is unknown. In this study, we induced mouse model via aortic constriction (TAC) to further explore pathological inflammasome-mediated pyroptosis potential therapeutic effects irisin. Cardiac significantly increased percentage apoptotic cells upregulated IL-1β, cleaved caspase-1, GSDMD-N that lie downstream inflammasome. Subsequently, was co-administered TAC mice or angiotensin II (Ang-II)-treated cardiomyocytes observe whether it could attenuate hypertrophy. We established direct association between found pharmacological genetic inhibition attenuated Furthermore, ectopic overexpression abrogated cardioprotective To summarize, factor hypertrophy, promising agent inhibits NLRP3-mediated cardiomyocytes.

Language: Английский

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Heat therapy: mechanistic underpinnings and applications to cardiovascular health

Journal of Applied Physiology, Journal Year: 2021, Volume and Issue: 130(6), P. 1684 - 1704

Published: April 1, 2021

Cardiovascular diseases (CVD) are the leading cause of death worldwide, and novel therapies drastically needed to prevent or delay onset CVD reduce societal healthcare burdens associated with these chronic diseases. One such therapy is “heat therapy,” chronic, repeated use hot baths saunas. Although using heat exposure improve health not a new concept, it has received renewed attention in recent years as growing number studies have demonstrated robust widespread beneficial effects on cardiovascular health. Here, we review existing literature, particular focus molecular mechanisms that underscore benefits this practice.

Language: Английский

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Knockout RAGE alleviates cardiac fibrosis through repressing endothelial-to-mesenchymal transition (EndMT) mediated by autophagy

Cell Death and Disease, Journal Year: 2021, Volume and Issue: 12(5)

Published: May 11, 2021

Endothelial-to-mesenchymal transition (EndMT) has been shown to contribute cardiac fibrosis and heart failure (HF). Recent studies have demonstrated that EndMT is regulated by autophagy, we previously showed suppression of excessive autophagy alleviation in HF mice with inactivated receptor for advanced glycation end products (RAGE). Thus, investigated whether reduced due RAGE knockout occurred inhibiting mediated autophagy. We found a decrease endothelial cells (CD31+/VE-Cadherin+) an increase co-expressing CD31 α-smooth muscle actin (α-SMA, myofibroblast marker) at 8 weeks tissue subjected transverse aortic constriction (TAC), which implied EndMT. Knockout decreased accompanied expression autophagy-related proteins (LC3BII/I Beclin 1), alleviated improved function TAC mice. Moreover, 3-methyladenine (3-MA) chloroquine (CQ), inhibitors attenuated EndMT, Importantly, induced AGEs could be blocked inhibitor vivo vitro. These results suggested AGEs/RAGE-autophagy-EndMT axis involved the development ameliorated through decreasing promising therapeutic strategy HF.

Language: Английский

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Mesenchymal stem cell-derived exosomes in cardiovascular and cerebrovascular diseases: From mechanisms to therapy

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 163, P. 114817 - 114817

Published: May 2, 2023

Cardiovascular and cerebrovascular diseases (CVDs) remain an intractable problem have high morbidity mortality worldwide, as well substantial health economic burdens, representing urgent clinical need. In recent years, the focus of research has shifted from use mesenchymal stem cells (MSCs) for transplantation to their secretory exosomes (MSC-exosomes) treatment numerous CVDs, including atherosclerosis, myocardial infarction (MI), heart failure (HF), ischemia/reperfusion (I/R), aneurysm, stroke. MSCs are pluripotent with multiple differentiation pathways that exert pleiotropic effects by producing soluble factors, most effective components which exosomes. MSC-exosomes considered be excellent promising cell-free therapy CVDs due higher circulating stability, improved biocompatibility, reduced toxicity, immunogenicity. addition, play critical roles in repairing inhibiting apoptosis, regulating inflammation, ameliorating cardiac remodeling, promoting angiogenesis. Herein, we describe knowledge about biological characteristics MSC-exosomes, investigate mechanism mediate therapeutic repair, summarize advances efficacy a view toward future applications.

Language: Английский

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Ginsenoside Rb1 promotes the activation of PPARα pathway via inhibiting FADD to ameliorate heart failure

European Journal of Pharmacology, Journal Year: 2023, Volume and Issue: 947, P. 175676 - 175676

Published: March 30, 2023

Language: Английский

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Role and molecular mechanisms of SGLT2 inhibitors in pathological cardiac remodeling (Review)

Molecular Medicine Reports, Journal Year: 2024, Volume and Issue: 29(5)

Published: March 11, 2024

Cardiovascular diseases are caused by pathological cardiac remodeling, which involves fibrosis, inflammation and cell dysfunction. This includes autophagy, apoptosis, oxidative stress, mitochondrial dysfunction, changes in energy metabolism, angiogenesis dysregulation of signaling pathways. These heart structure and/or function ultimately result failure. In an effort to prevent this, multiple cardiovascular outcome trials have demonstrated the benefits sodium‑glucose cotransporter type 2 inhibitors (SGLT2is), hypoglycemic drugs initially designed treat diabetes mellitus. SGLT2is include empagliflozin dapagliflozin, listed as guideline 2021 European Guidelines for Heart Failure 2022 American Association/American College Cardiology/Heart Society America Management. recent years, studies using animal models explored mechanisms remodeling. article reviews role remodeling induced different etiologies provide a further evaluation underlying inhibition SGLT2is, well development novel drug targets.

Language: Английский

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Baicalin alleviates angiotensin II‐induced cardiomyocyte apoptosis and autophagy and modulates the AMPK/mTOR pathway

Journal of Cellular and Molecular Medicine, Journal Year: 2024, Volume and Issue: 28(9)

Published: May 1, 2024

Abstract As a main extraction compound from Scutellaria baicalensis Georgi, Baicalin exhibits various biological activities. However, the underlying mechanism of on hypertension‐induced heart injury remains unclear. In vivo, mice were infused with angiotensin II (Ang II; 500 ng/kg/min) or saline using osmotic pumps, followed by intragastrically administrated (5 mg/kg/day) for 4 weeks. vitro, H9C2 cells stimulated Ang (1 μM) and treated (12.5, 25 50 μM). treatment significantly attenuated decrease in left ventricular ejection fraction fractional shortening, increase mass, systolic volume diastolic mice. Moreover, reversed 314 differentially expressed transcripts cardiac tissues mice, enriched multiple signalling pathways (including apoptosis, autophagy, AMPK/mTOR pathway). Consistently, alleviated II‐induced cell apoptosis vivo vitro. up‐regulation Bax, cleaved‐caspase 3, 9, down‐regulation Bcl‐2. Meanwhile, autophagosomes, restored autophagic flux, down‐regulated LC3II, Beclin 1, as well up‐regulated SQSTM1/p62 expression. Furthermore, autophagy inhibitor 3‐methyladenine autophagosomes Bcl‐2 expression after treated, which similar to co‐treatment Baicalin. reduced ratio p‐AMPK/AMPK, while increased p‐mTOR/mTOR. cardiomyocyte might be related inhibition pathway.

Language: Английский

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Astragali Radix−Notoginseng Radix et Rhizoma medicine pair prevents cardiac remodeling by improving mitochondrial dynamic balance

Chinese Journal of Natural Medicines, Journal Year: 2025, Volume and Issue: 23(1), P. 54 - 63

Published: Jan. 1, 2025

Language: Английский

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