Latest ArticlesCirsium souliei (Asteraceae) is a perennial medicinal herb of Cirsium with important medicinal and ecological values. Here, we sequenced the complete chloroplast (cp) genome of C. souliei based on high-throughput sequencing technology, then assembled and annotated it, and analysed the structure and characteristics of the cp genome. The result indicated that the cp genome of C. souliei was a typical quadripartite circular structure of 152 470 bp in length, and GC content was 37.7%. The cp genome of C. souliei encoded 134 genes, including 89 protein-coding genes, 37 tRNA genes and 8 rRNA genes. Meanwhile, we detected 188 simple sequence repeats (SSR) loci in the cp genome, which were mainly composed of mononucleotide repeats. Codon bias analysis showed that leucine (Leu) was the highest amino acids with frequency (10.51%), and there were 30 codons with the value of relative synonymous codon usage (RSCU) above one, of which mostly ended with A/U. Additionally, the result from phylogenetic analysis based on 46 cp genomes of Carduoideae showed that C. souliei and C. vulgare were sister species, and had the closest relationship with 100% bootstrap within Cirsium. This study provides theoretical basis for future studying genetic diversity, population genetic structure, systematics and evolution, and speciation mechanism.
In the process of evolution, pathogenic Streptococcus pyogenes secretes an immunoglobulin G-degrading enzyme IdeS which can specifically cleave the hinge region of immunoglobulin G in order to escape the immune response against the host. On the one hand, IdeS can be used for IgG fingerprinting as a tool enzyme combined with mass spectrometry technology. On the other hand, IdeS can be used to treat the antibody-responsive diseases produced by autoimmunity as a therapeutic protein. In this study, the backbone of plasmid pCold was used to construct two expression vectors of recombinant protein IdeS, which were heterologously expressed in Escherichia coli Shuffle T7. After purification by affinity chromatography, the recombinant IdeS activity was detected and their activity differences between the two were compared. Among them, the yield of the recombinant IdeS containing the His6-tag at the N-terminus was 4 mg·L-1, and the cleavage reaction with antibody IgG1 at 1∶200 (m/m) at 37 ℃ for 30 min could complete. However, the yield of the recombinant IdeS containing both the N-terminal His6 tag and the C-terminal silica affinity tag (silica bing peptide, SiBP) is 1.5 mg·L-1, and the degradation reaction with antibody IgG1 at 1∶20 (m/m) at 37 ℃ for 30 min could reach the end. The C-terminal fusion peptide has a great influence on the yield and activity of IdeS, which is not conducive to subsequent application in drug development. Above all, the recombinant IdeS containing the His6-tag at the N-terminus expressed by this system has high activity and can fully meet the needs of antibody drug development and mapping analysis of IgG.
Oxygen is vital for life. Redox stress is important in cell signal transduction, mediating many physiological and pathological processes such as aging, neurodegenerative diseases, metabolic diseases and tumors. Redox homeostasis maintainance is critical for promoting life health. In this paper, the lasting challenges during antioxidant research and development and the beyond main reasons were analyzed: including insufficient understanding of the physiological function of redox stress; excessive antioxidant, causing reductive stress; antioxidant strategies lacking specificity. Here the author proposed that cells and the body own precise redox nature, therefore, redox intervention strategies such as anti-oxidation should consider the "5R" principle, i.e. right species, right time, right place, right level, right target. Precision redox regulation is the future direction and precise redox medicine development is opening.
Ferroptosis is a novel type of cell death, which is distinguished from the traditional cell death pathways such as apoptosis, proptosis, necrosis and autophagy in terms of morphology, biochemistry and genetics. The main features of ferroptosis are the iron accumulation and lipid peroxidation. The regulation mechanism of ferroptosis involves glutathione metabolism, lipid peroxidation reactions and iron metabolism, which are closely related to the pathological process of tumor, aging, neurodegenerative diseases, ischemia reperfusion injury, cardiovascular and cerebrovascular diseases, kidney injury, hepatic fibrosis and so on. How to effectively study the role of ferroptosis regulation mechanism in the treatment of diseases becomes the hot spot and focus of the ferroptosis research. In recent years, with the in-depth study of ferroptosis, the identification, confirmation and the mechanism of ferroptosis have been developed significantly and have come forth continuously, in the meantime, techniques based on the morphology, biochemistry, molecular biology and genetics have been widely applied in the detection of ferroptosis. In order to deepen readers' understanding of ferroptosis and its detection methods, this paper will mainly review the current research progress on the detection methods and their application in ferroptosis, summarize and discuss their advantages and disadvantages in the detection of ferroptosis, this knowledge are crucial for better understanding and studying the biological function of ferroptosis.
The remodeling of phospholipid includes two processes: deacylation and reacylation. It realizes the conversion of nascent phospholipids to mature phospholipids by changing the length and types of fatty acids at specific sites of phospholipids, which is a key step in phospholipid metabolism. Phospholipids are not only the basic components of biological membranes, but also participate in the transduction of many molecular signals in cells. Therefore, phospholipid remodeling disorders can affect the structure and function of cell membranes, as well as the activity of membrane proteins, causing a series of intricate signaling cascades, and finally lead to many pathological changes including neurodegeneration. This paper reviews the basic process of phospholipid remodeling and the involvement of its key enzymes, calcium independent group VIA phospholipase A2 (iPLA2β), peroxiredoxin 6 (PRDX6), calcium independent group VIB phospholipase A2 (iPLA2γ) as well as acyl-CoA lysocardiolipin acyltransferase 1 (ALCAT1) in the pathology of Parkinson's disease. The mutations in the gene encoding iPLA2β, PLA2G6, have been widely reported to be directly related to hereditary Parkinson disease-14 (PARK14). Here we focus on the molecular mechanism of iPLA2β in the development of Parkinson's disease, mainly involving phospholipid fatty acid metabolism disorders, mitochondrial physiology abnormalities and α-synuclein aggregate formation and other aspects, which will help to understand the role of phospholipid remodeling in Parkinson's disease, and provide new clues for the development of new Parkinson's disease diagnosis and treatment strategies.
Immune checkpoints (ICs) are immunosuppressive molecules expressed on immune cells, which can regulate immune cells' activation. Immune checkpoint inhibitors (ICIs) which can block the interaction of immune checkpoints and their ligands, improve the cytotoxic effect of the immune system on tumor cells. Immunotherapy such as employing ICIs has gradually become a conventional therapeutic strategy for cancer treatment. However, the low response rate and the emergence of drug resistance have seriously affected the clinical efficacy of ICIs. Reactive oxygen species (ROS) are electronic reduction products of active oxygen, as well as natural by-products of cell metabolism, which can be used as regulators of intercellular signals. Tumor microenvironment (TME) is often in the state of oxidative stress (OS), which is the imbalance between oxidative system and antioxidant system. ROS can affect the interaction with its ligands by regulating the expression and activity of immune checkpoints in TME, thus affecting the anti-tumor effect of immune cells. Accumulating studies have shown that ROS could regulate tumor immune checkpoints through several pathways. Due to different types and stages of tumor, it would be clinical beneficial to understand the mechanistic link of ROS on tumor immune checkpoint, and choose appropriate ROS regulators combined with immune checkpoint inhibitors to maximize anti-tumor effects. This article reviews the common metabolic sources and characteristics of ROS, the regulatory effect and mechanism of ROS on tumor immune checkpoints and its therapeutic application.
Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that catalyzes the conversion of heme to CO, biliverdin, and iron, which together protect cells from oxidative and inflammatory damage and play an important role in maintaining cell homeostasis. In recent years, HO-1 has also been found to have antiviral biological effects, and the induced expression of HO-1 inhibits the replication of various viruses such as hepatitis C virus, hepatitis B virus, human immunodeficiency virus, dengue virus, ebolavirus, influenza A virus, Zika virus, severe acute respiratory syndrome coronavirus 2, human respiratory syncytial virus, hepatitis A virus and enterovirus 71. The inhibitory effect of HO-1 on these viruses involves three mechanisms, including direct inhibition of virus replication by HO-1 and its downstream products, enhancement of type I interferon responses in host cell, and attenuation of inflammatory damage caused by viral infection. This review focuses on the recent advances in the antiviral effect of HO-1 and its mechanism, which is expected to provide evidence for HO-1 as a potential target for antiviral therapy.
The pathogenesis of heart failure is a complex progression and associated with abnormal regulation of many signaling pathways. As a cofactor of hemoglobin, myoglobin, oxidative respiratory chain, DNA synthase and other important proteins, iron plays an indispensable role in myocardial energy metabolism. Recently, a large number of studies have shown that heart failure is related to the disorder of iron metabolism. Both iron deficiency and iron overload can lead to the development of a variety of cardiomyopathy, and even progress to heart failure. Iron metabolism could be a key target for the diagnosis, prevention and treatment of heart failure. Here, we review the basic process of iron metabolism and its mechanism in heart failure, expecting to provide new clues and evidence for the treatment of heart failure.
The iron and inflammation homeostasis are closely coupled, forming an integrated functional unit under physiological conditions. "Iron transport balance" has become the key mechanism to maintain iron homeostasis through bidirectional regulation of iron uptake and release and dynamic management of transmembrane concentration. It is also the physiological basis for the inflammatory balance between promotion and resolution. Under pathological conditions, represented by inflammatory bowel disease (IBD), disturbed iron transportation was highly involved in almost every step of inflammatory diseases. Therefore, the iron transporting rebalancing provides the mechanistic basis and effective approach for the normalization of inflammatory microenvironment. Macrophage is the key regulator of inflammation homeostasis and determinant for iron transport balance. Unfortunately, the current clinical transformation based on iron transport balance theory has still been insufficient. Sometimes, this strategy even showed high complexity and contradiction, severely restricting its clinical application. By summarizing the theoretical research progress of iron transport balance, especially its relevance to macrophage phenotypic polarization, this review aims to explore the therapeutic value in inflammation intervention by targeting iron transporting balance. This review will provide the necessary knowledge and hints for the research and development of candidate drugs in treating inflammatory diseases.
The discovery of regulatory cell death has led to new breakthroughs in the field of disease treatment. As a novel discovered regulatory cell death in the past decade, ferroptosis is characterized by abnormal increase of intracellular iron ions and peroxidative damage of cell membrane lipids, morphological features of mitochondrial volume reduction, increased mitochondrial membrane density, as well as mitochondria decrease or disappear. The mechanism of ferroptosis is mainly associated with factors such as iron metabolism disorder, lipid metabolism abnormality, amino acid antioxidant system imbalance and oxidative stress. Since the liver is the main organ of human body for storing iron ions, it is necessary to deeply investigate the mechanism of ferroptosis in liver diseases. Relevant studies have shown that ferroptosis plays different roles in various liver diseases and is closely related to the process of liver diseases, including drug-induced liver injury, alcoholic fatty liver disease, non-alcoholic fatty liver diseases, viral hepatitis, liver fibrosis and hepatocellular carcinoma. The aim of this review is to link ferroptosis and liver diseases, concentrating on the iron metabolism disorder, accumulation of lipid peroxides in cell membranes, imbalance of amino acid antioxidant system, hyperpolarization of mitochondrial membrane potential and its accumulation of lipid peroxides, oxidative stress-related transcription factors and other aspects. This review summarizes the regulatory mechanism, current situation and the roles of ferroptosis in liver diseases, in order to provide a new theoretical basis and ideas for the in-depth study of ferroptosis and the treatment of liver diseases.
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