miR-133: A Suppressor of Cardiac Remodeling?

Frontiers in Pharmacology, Год журнала: 2018, Номер 9

Опубликована: Авг. 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.

Язык: Английский

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

Acta Pharmacologica Sinica, Год журнала: 2018, Номер 39(7), С. 1100 - 1109

Опубликована: Март 22, 2018

Язык: 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, Год журнала: 2021, Номер 7(1)

Опубликована: Март 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.

Язык: Английский

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

Cell Death and Disease, Год журнала: 2021, Номер 12(5)

Опубликована: Май 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.

Язык: Английский

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Heat therapy: mechanistic underpinnings and applications to cardiovascular health

Journal of Applied Physiology, Год журнала: 2021, Номер 130(6), С. 1684 - 1704

Опубликована: Апрель 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.

Язык: Английский

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

Biomedicine & Pharmacotherapy, Год журнала: 2023, Номер 163, С. 114817 - 114817

Опубликована: Май 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.

Язык: Английский

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

European Journal of Pharmacology, Год журнала: 2023, Номер 947, С. 175676 - 175676

Опубликована: Март 30, 2023

Язык: 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, Год журнала: 2024, Номер 28(9)

Опубликована: Май 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.

Язык: Английский

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Metrnl: a promising biomarker and therapeutic target for cardiovascular and metabolic diseases

Cell Communication and Signaling, Год журнала: 2024, Номер 22(1)

Опубликована: Авг. 5, 2024

Modern human society is burdened with the pandemic of cardiovascular and metabolic diseases. Metrnl a widely distributed secreted protein in body, involved regulating glucose lipid metabolism maintaining system homeostasis. In this review, we present predictive therapeutic roles various diseases, including atherosclerosis, ischemic heart disease, cardiac remodeling, failure, hypertension, chemotherapy-induced myocardial injury, diabetes mellitus, obesity.

Язык: Английский

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HACE1 protects against myocardial ischemia–reperfusion injury via inhibition of mitochondrial fission in mice

BMC Cardiovascular Disorders, Год журнала: 2025, Номер 25(1)

Опубликована: Фев. 3, 2025

HECT domain and Ankyrin repeat Containing E3 ubiquitin-protein ligase 1 (HACE1) has been found to be associated with mitochondrial protection. Mitochondrial damage is a critical contributor myocardial ischemia–reperfusion injury (I/RI). However, little known about the role of HACE1 in pathogenesis I/RI. Male C57BL6 mice knockout (KO) were subjected 30 min ischemia via ligation left anterior descending artery, followed by 0, 2, 6, or 24 h reperfusion. The evaluated for histopathological injury, serum troponin I (cTnI) levels, oxidative stress apoptosis cardiac function. Prior ischemia, Mdivi-1(1.2 mg/kg) vehicle was administered. study revealed that increased expression ischemia/reperfusion (I/RI), resulted more severe dysfunction during I/R(P < 0.05). group exhibited higher levels malondialdehyde (MDA), greater fission, dissipation membrane potential (MMP), leading compared wild-type I/R group(P On other hand, further reduced superoxide dismutase (SOD) activity myocardium(P 0.05), supporting findings. adverse effects almost completely eliminated pharmacological blockade dynamin-related protein (Drp1) inhibitor, Mdivi-1, which inhibits fission Collectively, our data show I/RI downregulation Drp1 activation, causing cardiomyocytes undergo cell death. Therefore, could promising therapeutic target treatment

Язык: Английский

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