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Adverse remodeling after myocardial infarction (MI) result in heart failure and sudden cardiac death. Fibulin7 (FBLN7) is an adhesion protein excreted into the extracellular matrix that functions in multiple biological processes. However, whether and how FBLN7 affects post‐MI cardiac remodeling remains unclear. Here, the authors identify FBLN7 as a critical profibrotic regulator of adverse cardiac remodeling. They observe significantly upregulated serum FBLN7 levels in MI patients with left ventricular remodeling compared to those without MI. Microarray dataset analysis reveal FBLN7 is upregulated in human heart samples from patients with dilated and hypertrophic cardiomyopathy compared with non‐failing hearts. The authors demonstrate that FBLN7 deletion attenuated post‐MI cardiac remodeling, leading to better cardiac function and reduced myocardial fibrosis, whereas overexpression of FBLN7 results in the opposite effects. Mechanistically, FBLN7 binds to the epidermal growth factor receptor (EGFR) through its EGF‐like domain, together with the EGF‐like calcium‐binding domain, and induces EGFR autophosphorylation at tyrosine (Y) 1068 and Y1173, which activates downstream focal adhesion kinase/AKT signaling, thereby leading to fibroblast‐to‐myofibroblast transdifferentiation. In addition, FBLN7‐EGFR mediates this signal transduction, and the fibrotic response is effectively suppressed by the inhibition of EGFR activity. Taken together, FBLN7 plays an important role in cardiac remodeling and fibrosis after MI. [ABSTRACT FROM AUTHOR]

Intestinal flora plays an important role in atherosclerosis. Tongxinluo, as a multi-target Chinese medicine to improve atherosclerosis, whether it can improve atherosclerosis by affecting the intestinal flora is worth exploring. We established a vulnerable plaque model of atherosclerosis in New Zealand white rabbits by high cholesterol diet and balloon injury (HCB), and performed Tongxinluo intervention. We detected the level of inflammation by immunohistochemistry, Western Blot, and ELISA, analyzed plaque characteristics by calculating the vulnerability index, and analyzed the changes of gut microbiota and metabolites by 16S rRNA gene sequencing and untargeted metabolomic sequencing. The results showed that Tongxinluo intervention improved plaque stability, reduced inflammatory response, inhibited NLRP3 inflammatory pathway, increased the relative abundance of beneficial bacteria such as Alistipes which reduced by HCB, and increased the content of beneficial metabolites such as trans-ferulic acid in feces. Through correlation analysis, we found that some metabolites were significantly correlated with some bacteria and some inflammatory factors. In particular, the metabolite trans-ferulic acid was also significantly positively correlated with plaque stability. Our further studies showed that trans-ferulic acid could also inhibit the NLRP3 inflammatory pathway. In conclusion, Tongxinluo can improve plaque stability and reduce inflammation in atherosclerotic rabbits, which may be achieved by modulating intestinal flora and intestinal metabolism. Our study provides new views for the role of Tongxinluo in improving atherosclerotic vulnerable plaque, which has important clinical significance. [ABSTRACT FROM AUTHOR]

Lymphangiogenesis is possibly capable of attenuating hypertension‐induced cardiac injury. Sirtuin 3 (SIRT3) is an effective mitochondrial deacetylase that has the potential to modulate this process; however, its role in hypertension‐induced cardiac lymphangiogenesis to date has not been investigated. Our experiments were performed on 8‐week‐old wild‐type (WT), SIRT3 knockout (SIRT3‐KO) and SIRT3 overexpression (SIRT3‐LV) mice infused with angiotensin II (Ang II) (1000 ng/kg per minute) or saline for 28 days. After Ang II infusion, SIRT3‐KO mice developed a more severe cardiac remodelling, less lymphatic capillaries and lower expression of lymphatic marker when compared to wild‐type mice. In comparison, SIRT3‐LV restored lymphangiogenesis and attenuated cardiac injury. Furthermore, lymphatic endothelial cells (LECs) exposed to Ang II in vitro exhibited decreased migration and proliferation. Silencing SIRT3 induced functional decrease in LECs, while SIRT3 overexpression LECs facilitated. Moreover, SIRT3 may up‐regulate lymphangiogenesis by affecting vascular endothelial growth factor receptor 3 (VEGFR3) and ERK pathway. These findings suggest that SIRT3 could promote lymphangiogenesis and attenuate hypertensive cardiac injury. [ABSTRACT FROM AUTHOR]

Context: Sunitinib (SU) is a multi-targeted tyrosine kinase inhibitor anticancer agent whose clinical use is often limited by cardiovascular complications. Trimetazidine (TMZ) is an anti-angina agent that has been demonstrated cardioprotective effects in numerous cardiovascular conditions, but its potential effects in SU-induced cardiotoxicity have not been investigated. Objective: This study investigates the effect of TMZ in sunitinib-induced cardiotoxicity in vivo and in vitro and molecular mechanisms. Materials and methods: Male 129S1/SvImJ mice were treated with vehicle, SU (40 mg/kg/d) or SU and TMZ (20 mg/kg/d) via oral gavage for 28 days, and cardiovascular functions and cardiac protein expressions were examined. H9c2 cardiomyocytes were treated with vehicle, SU (2–10 μM) or SU and TMZ (40–120 μM) for 48 h, and cell viability, apoptosis, autophagy, and protein expression was tested. Results: SU induces hypertension (systolic blood pressure [SBP] + 28.33 ± 5.00 mmHg) and left ventricular dysfunction (left ventricular ejection fraction [LVEF] − 11.16 ± 2.53%) in mice. In H9c2 cardiomyocytes, SU reduces cell viability (IC50 4.07 μM) and inhibits the AMPK/mTOR/autophagy pathway (p < 0.05). TMZ co-administration with SU reverses SU-induced cardiotoxicity in mice (SBP − 23.75 ± 4.69 mmHg, LVEF + 10.95 ± 3.317%), alleviates cell viability loss in H9c2 cardiomyocytes (p < 0.01) and activates the AMPK/mTOR/autophagy pathway in vivo (p < 0.001) and in vitro (p < 0.05). Discussion and conclusions: Our results suggest TMZ as a potential cardioprotective approach for cardiovascular complications during SU regimen, and potentially for cardiotoxicity of other anticancer chemotherapies associated with cardiomyocyte autophagic pathways. [ABSTRACT FROM AUTHOR]

We report the fabrication of the AlV 3 O 9 nanoflowers, which is then used as cathode and anode materials for high-performance lithium ion batteries. The existence of Al 3+ in the vanadium oxygen interlayers reduces electrochemical impedance and improves lithium ion diffusion coefficient of aluminum vanadates, resulting in the enhanced electrochemical performance. Electrochemical measurements show that the AlV 3 O 9 nanoflowers demonstrate good electrochemical performance as cathode and anode materials. Specially, the anode performance of aluminum vanadate is evaluated for the first time. A high capacity of 843 mA h g −1 for second cycle at 100 mA g −1 is obtained for AlV 3 O 9 anode. Even cycled at 1000 mA g −1 , it can maintain a high capacity of 295 mA h g −1 up to 500 cycles. The good performance of AlV 3 O 9 nanoflowers may be ascribed to their 3D hierarchical structure and the conductivity improvement by the incorporation of aluminum ions. [ABSTRACT FROM AUTHOR]

Groundwork on cyanobacterial external layers is crucial for an improved understanding of the persistent dominance of cyanobacteria in freshwaters. In this study, the role of two morphotypes of external layers in Microcystis and Nostoc in mass transfer and instantaneous temperature shock were explored by noninvasive microtest technology (NMT) after a series of pretreatments, to obtain the external layers retained or stripped samples. The results showed no statistical influence on photosynthetic activity between retained and stripped samples in both Microcystis and Nostoc. External-layer-retaining strains had higher net O2 effluxes than stripped strains. Moreover, the net NH4+ influx was significantly higher for the sheath retaining Nostoc than for the stripped sample, indicating that external layers might be an important feature driving mass transfer in cyanobacteria. However, the role of slime in NH4+ absorption was limited compared with that of sheath. In addition, external-layer-retaining strains exhibited a longer response time to instantaneous temperature shock, greater net O2 effluxes at a 4 °C shock and lower net O2 influx at a 35 °C shock, which were interpreted as reflecting a tolerance to temperature fluctuation over short time scales via a buffer function of external layers to stabilize cell activity, ameliorating the efficiency of photosynthesis and respiration. These results advance current knowledge regarding the external layers, especially the dense sheath, involved in the mass transfer in cyanobacteria, and provide new clues concerning the adaptive strategies of cyanobacteria under global climate changes. [ABSTRACT FROM AUTHOR]

Cu3V2O7(OH)2·2H2O materials have been synthesized by a facile hydrothermal route without any templates. The XRD results showed that the as-prepared materials are of high crystallinity and high purity. The Cu3V2O7(OH)2·2H2O material prepared at 190°C for 12h is composed of a large quantity of well-separated nanoparticles with the diameters ranging from 50nm to 200nm. The results of electrochemical measurement indicate that the Cu3V2O7(OH)2·2H2O material exhibits high initial discharge capacity and high-rate capability. A high specific discharge capacity of 544, 503, 475, 458 and 429mAhg−1 can be achieved at different current densities of 10, 20, 30, 50 and 100mAg−1, respectively. The superior electrochemical properties suggest that they are a promising cathode material for implantable cardioverter defibrillators (ICDs). [ABSTRACT FROM AUTHOR]

Heart failure caused by pressure overload is one of the leading causes of heart failure worldwide, but its pathological origin remains poorly understood. It remains critical to discover and find new improvements and treatments for pressure overload-induced heart failure. According to previous studies, mitochondrial dysfunction and myocardial interstitial fibrosis are important mechanisms for the development of heart failure. The oligopeptide Szeto-Schiller Compound 31 (SS31) can specifically interact with the inner mitochondrial membrane and affect the integrity of the inner mitochondrial membrane. Whether SS31 alleviates pressure overload-induced heart failure through the regulation of mitochondrial fusion has not yet been confirmed. We established a pressure-overloaded heart failure mouse model through TAC surgery and found that SS31 can significantly improve cardiac function, reduce myocardial interstitial fibrosis, and increase the expression of optic atrophy-associated protein 1 (OPA1), a key protein in mitochondrial fusion. Interestingly, the role of SS31 in improving heart failure and reducing fibrosis is inseparable from the presence of sirtuin3 (Sirt3). We found that in Sirt3KO mice and fibroblasts, the effects of SS31 on improving heart failure and improving fibroblast transdifferentiation were disappeared. Likewise, Sirt3 has direct interactions with proteins critical for mitochondrial fission and fusion. We found that SS31 failed to increase OPA1 expression in both Sirt3KO mice and fibroblasts. Thus, SS31 can alleviate pressure overload-induced heart failure through Sirt3-mediated mitochondrial fusion. This study provides new directions and drug options for the clinical treatment of heart failure caused by pressure overload., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Suo, Qi, Liu, Zhang, Li, Yan, Zhang, Ti, Chen and Bu.)