SUMOylation of TP53INP1 is involved in miR-30a-5p-regulated heart senescence.

Heart senescence is critical for cardiac function. This study aimed to characterize the role and mechanism of action of miR-30a-5p in cardiac senescence. miR-30a-5p was downregulated in aged mouse hearts and neonatal rat cardiomyocytes (NRCMs).

The gut microbiotas with metabolites regulate the protective role of miR-30a-5p in myocardial infarction.

Introduction: Gut microbial homeostasis is closely associated with myocardial infarction (MI). However, little is known about how gut microbiota influences miRNAs-regulated MI.

Objectives: This study aims to elucidate the connections between miR-30a-5p, MI, gut microbiota, and gut microbial metabolite-related pathways, to explore potential strategy for preventing and treating MI.

Deletion of endothelial IGFBP5 protects against ischaemic hindlimb injury by promoting angiogenesis.

Background: Angiogenesis is critical for forming new blood vessels from antedating vascular vessels. The endothelium is essential for angiogenesis, vascular remodelling and minimisation of functional deficits following ischaemia. The insulin-like growth factor (IGF) family is crucial for angiogenesis.

Pyroptosis and mitochondrial function participated in miR-654-3p-protected against myocardial infarction.

Myocardial infarction (MI) is one of the leading causes of heart failure with highly complicated pathogeneses. miR-654-3p has been recognized as a pivotal regulator of controlling cell survival. However, the function of miR-654-3p in cardiomyocytes and MI has yet to be reported.

NEDD4L is a promoter for angiogenesis and cell proliferation in human umbilical vein endothelial cells.

Dysregulated angiogenesis leads to neovascularization, which can promote or exacerbate various diseases. Previous studies have proved that NEDD4L plays an important role in hypertension and atherosclerosis. Hence, we hypothesized that NEDD4L may be a critical regulator of endothelial cell (EC) function.

Bradykinin-pretreated Human cardiac-specific c-kit Cells Enhance Exosomal miR-3059-5p and Promote Angiogenesis Against Hindlimb Ischemia in mice.

Background: Protection of cardiac function following myocardial infarction was largely enhanced by bradykinin-pretreated cardiac-specific c-kit (BK-c-kit) cells, even without significant engraftment, indicating that paracrine actions of BK-c-kit cells play a pivotal role in angiogenesis. Nevertheless, the active components of the paracrine actions of BK-c-kit cells and the underlying mechanisms remain unknown. This study aimed to define the active components of exosomes from BK-c-kit cells and elucidate their underlying protective mechanisms.

The Reverse Fitness Deficiency by Activating a Novel β-Glucosidase Under Low Osmostress.

Bacteria can withstand various types of environmental osmostress. A sudden rise in osmostress affects bacterial cell growth that is countered by activating special genes. The change of osmostress is generally a slow process under the natural environment.

Acacetin attenuates diabetes-induced cardiomyopathy by inhibiting oxidative stress and energy metabolism via PPAR-α/AMPK pathway.

Diabetic cardiomyopathy seriously affects the life quality of diabetic patients and can lead to heart failure and death in severe cases. Acacetin was reported to be an anti-oxidant and anti-inflammatory agent in several cardiovascular diseases. However, the effect of acacetin on diabetic cardiomyopathy was not understood.

Acacetin alleviates myocardial ischaemia/reperfusion injury by inhibiting oxidative stress and apoptosis via the Nrf-2/HO-1 pathway.

Context: Acacetin is a natural source of flavonoids with anti-inflammatory and antioxidant effects.

Objective: This study determines acacetin's protective effect and mechanism on myocardial ischaemia/reperfusion (I/R) injury.

Materials And Methods: Sprague-Dawley rats were divided into sham and I/R injury and treatment with acacetin.

Acacetin ameliorates cardiac hypertrophy by activating Sirt1/AMPK/PGC-1α pathway.

Cardiac hypertrophy is a major risk factor for developing heart failure. This study investigates the effects of the natural flavone acacetin on myocardial hypertrophy in cellular level and whole animals. In cardiomyocytes from neonatal rat with hypertrophy induced by angiotensin II (Ang II), acacetin at 0.

Concanavalin A promotes angiogenesis and proliferation in endothelial cells through the Akt/ERK/Cyclin D1 axis.

Context: Concanavalin A (Con A) exhibited multiple roles in cancer cells. However, the role of Con A in endothelial cells was not reported.

Objective: Our present study investigated the potential angiogenic role of Con A in endothelial cells and ischaemic hind-limb mice.

Ubiquitinated ligation protein NEDD4L participates in MiR-30a-5p attenuated atherosclerosis by regulating macrophage polarization and lipid metabolism.

MiR-30a-5p plays an important role in various cardiovascular diseases, but its effect in atherosclerosis has not been reported. Apolipoprotein E-deficient (Apo E) mice were used to investigate the role of miR-30a-5p in atherosclerosis, and the underlying mechanism was investigated and . The fluorescence hybridization test revealed that miR-30a-5p was expressed in Apo E mice lesions.

Cardiac senescence is alleviated by the natural flavone acacetin via enhancing mitophagy.

Cardiac senescence is associated with cardiomyopathy which is a degenerative disease in the aging process of the elderly. The present study investigates using multiple experimental approaches whether the natural flavone acacetin could attenuate myocardial senescence in C57/BL6 mice and H9C2 rat cardiac cells induced by D-galactose. We found that the impaired heart function in D-galactose-induced accelerated aging mice was improved by oral acacetin treatment in a dose-dependent manner.

Acacetin exerts antioxidant potential against atherosclerosis through Nrf2 pathway in apoE Mice.

Oxidative stress has a considerable influence on endothelial cell dysfunction and atherosclerosis. Acacetin, an anti-inflammatory and antiarrhythmic, is frequently used in the treatment of myocarditis, albeit its role in managing atherosclerosis is currently unclear. Thus, we evaluated the regulatory effects of acacetin in maintaining endothelial cell function and further investigated whether the flavonoid could attenuate atherosclerosis in apolipoprotein E deficiency (apoE ) mice.

Doxorubicin cardiomyopathy is ameliorated by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules.

Doxorubicin cardiotoxicity is frequently reported in patients undergoing chemotherapy. The present study investigates whether cardiomyopathy induced by doxorubicin can be improved by the natural flavone acacetin in a mouse model and uncovers the potential molecular mechanism using cultured rat cardiomyoblasts. It was found that the cardiac dysfunction and myocardial fibrosis induced by doxorubicin were significantly improved by acacetin in mice with impaired Nrf2/HO-1 and Sirt1/pAMPK molecules, which is reversed by acacetin treatment.

Regulation of the TRPC1 channel by endothelin-1 in human atrial myocytes.

Background: Our recent study demonstrated that the nonselective cation current mediated by the transient receptor potential canonical 1 (TRPC1) channel is activated by endothelin-1 (ET-1) in human atrial myocytes; however, the related signal molecules involved are unknown.

Objective: The purpose of this study was to investigate how the TRPC1 channel is regulated by ET-1 and whether it is upregulated in human atria from patients with atrial fibrillation (AF).

Methods: Whole-cell patch technique and molecular biology techniques were used in the study.

Bradykinin-mediated Ca signalling regulates cell growth and mobility in human cardiac c-Kit progenitor cells.

Our recent study showed that bradykinin increases cell cycling progression and migration of human cardiac c-Kit progenitor cells by activating pAkt and pERK1/2 signals. This study investigated whether bradykinin-mediated Ca signalling participates in regulating cellular functions in cultured human cardiac c-Kit progenitor cells using laser scanning confocal microscopy and biochemical approaches. It was found that bradykinin increased cytosolic free Ca ( ) by triggering a transient Ca release from ER IP3Rs followed by sustained Ca influx through store-operated Ca entry (SOCE) channel.

Circulating miRNA-302 family members as potential biomarkers for the diagnosis of acute heart failure.

Aim: To explore circulating miRNA-302 family members for acute heart failure (AHF) diagnosis.

Methods: Three groups of subjects, in other words, AHF patients, AHF free patients and healthy controls were recruited. Circulating levels of miR-302 family members were measured and analyzed for AHF diagnosis.

The Natural Flavone Acacetin Confers Cardiomyocyte Protection Against Hypoxia/Reoxygenation Injury via AMPK-Mediated Activation of Nrf2 Signaling Pathway.

The present study investigates the potential signal pathway of acacetin in cardioprotection against ischemia/reperfusion injury using an hypoxia/reoxygenation model in primary cultured neonatal rat cardiomyocytes and H9C2 cardiomyoblasts. It was found that acacetin (0.3-3 μM) significantly decreased the apoptosis and reactive oxygen species production induced by hypoxia/reoxygenation injury in cardiomyocytes and H9C2 cardiomyoblasts via reducing the pro-apoptotic proteins Bax and cleaved-caspase-3 and increasing the anti-apoptotic protein Bcl-2.

Clemizole hydrochloride blocks cardiac potassium currents stably expressed in HEK 293 cells.

Background And Purpose: Clemizole, a histamine H receptor antagonist has a potential therapeutic effect on hepatitis C infection and also potently inhibits TRPC5 ion channels. The aim of the present study was to investigate whether clemizole blocks cardiac K currents and thus affects cardiac repolarization.

Experimental Approach: Whole-cell patch techniques was used to examine the effects of clemizole on hERG channel current, I and K 1.

Hydrodynamics-based delivery of an interleukin-1 receptor II fusion gene ameliorates rat autoimmune myocarditis by inhibiting IL-1 and Th17 cell polarization.

Type II interleukin-1 receptor (IL-1RII) is a non-signaling decoy receptor that blocks the activity of interleukin-1 (IL-1), a pro-inflammatory cytokine involved in experimental autoimmune myocarditis (EAM). The aim of this study was to examine the effects of hydrodynamics-based delivery of a recombinant plasmid encoding IL-1RII-Ig and to elucidate the role of IL-1RII in EAM rats. Rats were immunized on day 0 and injected with a recombinant plasmid encoding IL-1RII-Ig or pCAGGS-SP-Ig (control plasmid) on day 6.