Recently, mounting evidence indicates that N6‐methyladenosine (m6A) modification functions as a pivotal posttranscriptional modification that regulates noncoding RNA biogenesis to influence the progression of multiple diseases. However, whether m6A modification is involved in aortic dissection (AD) development has never been reported. Meanwhile, numerous studies have shown that AngII‐induced inflammatory damage and excessive apoptosis of human aortic smooth muscle cells (HASMCs) are the crucial pathological features of AD development. Therefore, in this study, we intended to explore whether m6A modification can regulate AD progression by influencing the damage effects of AngII on HASMCs and elucidate the underlying mechanisms. Firstly, we screened and confirmed the high expression of alkylation repair homolog protein 5 (ALKBH5), a key m6A demethylase, in aortic tissues from AD patients, indicating that m6A modification may indeed be involved in AD progression. Subsequently, we demonstrated that ALKBH5 can exacerbate the AngII‐induced HASMC inflammatory injury as well as apoptosis and shorten the survival time of AngII‐infused mice. Mechanistically, we revealed that lncRNA TMPO‐AS1 is a downstream target for ALKBH5 to affect AD progression in vitro and vivo. Meanwhile, we confirmed that ALKBH5‐mediated m6A demethylation downregulates lnc‐TMPO‐AS1 by decreasing the stability of its nascent. Further, we demonstrated that lnc‐TMPO‐AS1 exhibits its functions in HASMCs, at least partly, through downregulating IRAK4 at the epigenetic level by combining with EZH2. Finally, the direct positive correlation between ALKBH5 and IRAK4 in terms of the expression level and biological function was confirmed, which further enforced the preciseness and correctness of our findings. In conclusion, our study demonstrated that ALKBH5 aggravates AD by promoting inflammatory response and apoptosis of HASMCs via regulating lnc‐TMPO‐AS1/EZH2/IRAK4 signals in an m6A modification manner and may provide a novel molecular basis for subsequent researchers to searching for novel therapeutic approaches to improve the health of patients fighting AD and other cardiovascular diseases.
Iron deficiency (ID) is a global nutritional deficiency that was shown to be involved in the pathogenesis of aortic aneurysm and dissection (AAD) in our previous studies. Some studies suggested that mitochondrial dynamics was involved in the apoptosis and phenotypic transformation of vascular smooth muscle cells (VSMCs). However, little is known about the role of mitochondrial dynamics in aortic medial degeneration (AMD) promoted by an iron deficient diet. The present study investigated the effect of ID on the phenotypic transformation of VSMCs, the progression of AMD, and the underlying mechanism. The expression of p-Drp1 (Ser616) and Fis1 was markedly upregulated in the aortic media of AAD patients and ApoE-/- mice with subcutaneous AngII osmotic pumps. ID facilitated the formation of mitochondria-associated endoplasmic reticulum membranes (MAMs), which triggered excessive mitochondrial fission, induced the phenotypic transformation of VSMCs, and ultimately accelerated the progression of AMD. Furthermore, the present study indicated that an inhibitor of Drp1 could partially reverse this process. Maintaining iron balance in the human body may prevent the development of AAD.
Mangiferin is a naturally occurring xanthone C-glycoside that is widely found in various plants. Previous studies have reported that mangiferin inhibits tumor cell proliferation and migration. Excessive proliferation and migration of vascular smooth muscle cells (SMCs) is associated with neointimal hyperplasia in coronary arteries. However, the role and mechanism of mangiferin action in neointimal hyperplasia is still unknown. In this study, a mouse carotid artery ligation model was established, and primary rat smooth muscle cells were isolated and used for mechanistic assays. We found that mangiferin alleviated neointimal hyperplasia, inhibited proliferation and migration of SMCs, and promoted platelets derive growth factors-BB- (PDGF-BB-) induced contractile phenotype in SMCs. Moreover, mangiferin attenuated neointimal formation by inhibiting mitochondrial fission through the AMPK/Drp1 signaling pathway. These findings suggest that mangiferin has the potential to maintain vascular homeostasis and inhibit neointimal hyperplasia.
In order to improve the efficiency of photovoltaic array, which need maximum tracing power. Perturbation and observation method has become one of the algorithm of the wide range research because of its simple and easy. But the traditional P&O will be oscillation in near the maximum power point due to its fixed step disturbance and leads to some loss of power and in certain circumstances and incorrect judgment will be in steady state. In order to overcome these shortcomings, a variety of improved methods are proposed, and the main improvements of those are summarized. Some simulation experiments have been done for these methods, and these methods are proved to be feasible.
Heart transplantation (HT) is the only effective treatment for end-stage heart failure because it can effectively improve the survival rate and quality of life of patients with heart failure. Artesunate (ART) is an artemisinin derivative, with good water solubility and higher oral bioavailability. The main aim of this study was to determine the role of ART in HT mice.In animal experiments, mice were divided into the control group, HT group, low ART+HT group, and high ART+HT group. Next, inflammatory cell infiltration, oxidative stress injury, and myocardial cell apoptosis were determined in heart tissue. The proportion of multiple lymphocytes in spleen and lymph nodes was then determined using flow cytometry. In addition, cell experiments were conducted to determine the changes in expression of surface maturation markers of BMDC and changes in intracellular reactive oxygen species after LPS stimulation. Finally, western blot analysis was performed to determine the levels of endoplasmic reticulum stress-related proteins (CHOP/ATF4/PERK).The survival time of mice in the ART treatment group was significantly prolonged and was positively correlated with the dose. In animal experiments, ART significantly reduced inflammatory cell infiltration in heart tissue and the proportion of CD4+CD8+ T cells in spleens and lymph nodes. Moreover, ART treatment lowered the 8-OHdg in hearts and myocardial apoptosis. In cell experiments, ART treatment slowed down the development and maturation of BMDCs by inhibiting the expression of endoplasmic reticulum stress-related proteins. Furthermore, the treatment alleviated the oxidative stress damage of BMDCs.ART can inhibit maturation of dendritic cells through the endoplasmic reticulum stress signaling pathway, thereby alleviating acute rejection in mice after heart transplantation.
Despite decades of study into aortic dissection (AD), a lethal cardiovascular emergency due to a tear in the aorta intima or bleeding within the aortic wall, leading to the separation of the different layers of it, the factors that influence its progression and the deeper regulatory mechanisms remain poorly understood. Nowadays, with the maturity of N6-methyladenosine (m6A) sequence technology, m6A modification, one type of RNA epigenesis, has gradually become a new research hotspot for epigenetic molecular regulation. Especially recently, increasing evidence has revealed that m6A modification functions as a pivotal post-transcriptional modification to influence the progression of multiple diseases. Based on these findings, it is reasonable to speculate that m6A modification may affect the onset and progression of AD. To explore the validity of our conjecture and to elucidate its underlying molecular mechanism of action, we conducted the present study. In this study, we found that KIAA1429 is downregulated while ALKBH5 is upregulated in aortic tissues from AD patients. Furthermore, gain- and loss-of-function studies showed that KIAA1429 and ALKBH5 can oppositely regulate HASMC proliferation, HAEC apoptosis, and AD progression in AngII-infused mice. Mechanistically, we demonstrated that KIAA1429/ALKBH5-mediated m6A modifications can regulate the processing of pri-miR-143-3p through interacting with the microprocessor protein DGCR8, thus indirectly regulating the downstream target gene of mature miR-143-3p, DDX6, to perform their biological functions in vitro and in vivo . Our findings have revealed a novel connection between m6A modification and AD progression and may provide a novel molecular basis for subsequent researchers to search for novel therapeutic approaches to improve the health of patients struggling with AD.
Summary Energy is the cornerstone of the existence and development of modern society. The energy consumption continues to increase, and the ensuing environmental pollution and increasing lack of traditional energy sources have also become the world's most concerned issues. The emergence of new energy has eased the current unfavorable situation. Among them, distributed photovoltaic (PV) power generation has been favored because of its abundant resources and no geographical restrictions. However, due to the scattered construction of solar PV power stations, it is not easy to manage. Therefore, research and development of PV remote monitoring systems for unified monitoring and management of PV power stations. In addition, the problem of solar cell output efficiency is also an important reason that restricts the utilization of solar energy. Improving the output efficiency of the battery based on the existing solar cell conversion efficiency is also a focus of current research. Based on the above background, the research content of this article is the network communication monitoring system for distributed PV power generation systems. This article first conducts the overall design of the PV remote monitoring system, constructs the system's distributed design structure, and divides the underlying hardware part of the system into control modules and transmission. According to the application requirements, the STM32 series single‐chip microcomputer is selected as the controller of the system control module and the transmission module. The hardware circuit design and software process implementation of the system are studied to realize the data collection, MPPT control, and remote data transmission of the photovoltaic system. Features: Finally, through experimental simulation, it was verified that the light intensity increased from 600 to 800 W/m 2 , and the output current of the inverter increased accordingly. The output current of the distributed PV power generation system was directly proportional to the change of the light intensity. The designed system is feasible.
Abstract In order to improve the friendliness of the grid connection of new energy power generation, the new energy photovoltaic (PV) unit is equivalent to a synchronous generator in the power system and a virtual synchronous generator (VSG)-controlled PV energy storage complementary grid-connected power generation system model is established and studied to analyze the VSG. When power is supplied to the load together with the power grid, the energy storage unit inside the VSG will release and store the electrical energy according to the fluctuation of the PV output, which plays the role of the adjustment of the prime mover; in the case of load power fluctuations, and power grid assume the corresponding active power regulation according to their capacity. The amount of active power adjustment to jointly and maintain the power balance inside the system under the condition of fluctuating load power. The overall system architecture and control strategy of PV grid-connected inverter based on VSG algorithm are proposed. The PV-VSG proposed here not only takes into account the maximum power point tracking control but also has independent participation in the power supply. A series of characteristics of synchronous generators, such as network frequency modulation voltage regulation and inertia damping, can effectively improve the new energy PV power generation system and promote the new energy consumption. The results of system simulation and field demonstration operation fully show the effectiveness and correctness of the proposed control strategy based on VSG algorithm.
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