Cytokine & Growth Factor Reviews最新文献

Myeloid-derived growth factor (MYDGF) is a paracrine protein produced by bone marrow-derived monocytes and macrophages. Current research shows that it has protective effects on the cardiovascular system, such as repairing heart tissue after myocardial infarction, enhancing cardiomyocyte proliferation, improving cardiac regeneration after myocardial injury, regulating proliferation and survival of endothelial cells, reducing endothelial cell damage, resisting pressure overload-induced heart failure, as well as protecting against atherosclerosis. Furthermore, regarding the metabolic diseases, MYDGF has effects of improving type 2 diabetes mellitus, relieving non-alcoholic fatty liver disease, alleviating glomerular diseases, and resisting osteoporosis. Herein, we will discuss the biology of MYDGF and its effects on cardiovascular and metabolic diseases.

Cell-to-cell communication mediated by Extracellular Vesicles (EVs) is a novel and emerging area of research, especially during pregnancy, in which placenta derived EVs can facilitate the feto-maternal communication. EVs comprise a heterogeneous group of vesicle sub-populations with diverse physical and biochemical characteristics and originate by specific biogenesis mechanisms. EVs transfer molecular cargo (including proteins, nucleic acids, and lipids) between cells and are critical mediators of cell communication. There is growing interest among researchers to explore into the molecular cargo of EVs and their functions in a physiological and pathological context. For example, inflammatory mediators such as cytokines are shown to be released in EVs and EVs derived from immune cells play key roles in mediating the immune response as well as immunoregulatory pathways. Pregnancy complications such as gestational diabetes mellitus, preeclampsia, intrauterine growth restriction and preterm birth are associated with altered levels of circulating EVs, with differential EV cargo and bioactivity in target cells. This implicates the intriguing roles of EVs in reprogramming the maternal physiology during pregnancy. Moreover, the capacity of EVs to carry bioactive molecules makes them a promising tool for biomarker development and targeted therapies in pregnancy complications. This review summarizes the physiological and pathological roles played by EVs in pregnancy and pregnancy-related disorders and describes the potential of EVs to be translated into clinical applications in the diagnosis and treatment of pregnancy complications.

Interleukin (IL)− 33, a nuclear factor and pleiotropic cytokine of the IL-1 family, is gaining attention owing to its important role in chronic inflammatory and autoimmune diseases. This review extends our knowledge of the effects exerted by IL-33 on target cells by binding to its specific receptor serum stimulation-2 (ST2). Depending on the tissue context, IL-33 performs multiple functions encompassing host defence, immune response, initiation and amplification of inflammation, tissue repair, and homeostasis. The levels and activity of IL-33 in the body are controlled by complex IL-33-targeting regulatory pathways. The unique temporal and spatial expression patterns of IL-33 are associated with host homeostasis and the development of immune and inflammatory disorders. Therefore, understanding the origin, function, and processes of IL-33 under various conditions is crucial. This review summarises the regulatory mechanisms underlying the IL-33/ST2 signalling axis and its potential role and clinical significance in immune and inflammatory diseases, and discusses the current complex and conflicting findings related to IL-33 in host responses.

The vigorous spread of SARS-CoV-2 resulted in the rapid infection of millions of people worldwide and devastation of not only public healthcare, but also social, educational, and economic infrastructures. The evolution of SARS-CoV-2 over time is due to the mutations that occurred in the genome during each replication. These mutated forms of SARS-CoV-2, otherwise known as variants, were categorized as variants of interest (VOI) or variants of concern (VOC) based on the increased risk of transmissibility, disease severity, immune escape, decreased effectiveness of current social measures, and available vaccines and therapeutics. The swift development of COVID-19 vaccines has been a great success for biomedical research, and billions of vaccine doses, including boosters, have been administered worldwide. BNT162b2 vaccine (Pfizer–BioNTech), mRNA-1273 (Moderna), ChAdOx1 nCoV-19 (AstraZeneca), and Janssen (Johnson & Johnson) are the four major COVID-19 vaccines that received early regulatory authorization based on their efficacy. However, some SARS-CoV-2 variants resulted in higher resistance to available vaccines or treatments. It has been four years since the first reported infection of SARS-CoV-2, yet the Omicron variant and its subvariants are still infecting people worldwide. Despite this, COVID-19 vaccines are still expected to be effective at preventing severe disease, hospitalization, and death from COVID. In this review, we provide a comprehensive overview of the COVID-19 pandemic focused on evolution of VOC and vaccination strategies against them.

Fibrosis is a pathological condition characterized by the excessive deposition of extracellular matrix components in tissues and organs, leading to progressive architectural remodelling and contributing to the development of various diseases. Osteopontin (OPN), a highly phosphorylated glycoprotein, has been increasingly recognized for its involvement in the progression of tissue fibrosis. This review provides a comprehensive overview of the genetic and protein structure of OPN and focuses on our current understanding of the role of OPN in the development of fibrosis in the lungs and other tissues. Additionally, special attention is given to the potential of OPN as a biomarker and a novel therapeutic target in the treatment of fibrosis.

Innate lymphoid cells (ILCs), a growing class of immune cells, imitate the appearance and abilities of T cells. However, unlike T cells, ILCs lack acquired antigen receptors, and they also do not undergo clonal selection or proliferation in response to antigenic stimuli. Despite lacking antigen-specific receptors, ILCs respond quickly to signals from infected or damaged tissues and generate an array of cytokines that regulate the development of adaptive immune response. ILCs can be categorized into four types based on their signature cytokines and transcription factors: ILC1, ILC2, ILC3 (including Lymphoid Tissue inducer- LTi cells), and regulatory ILCs (ILCregs). ILCs play key functions in controlling and resolving inflammation, and variations in their proportion are linked to various pathological diseases including cancer, gastrointestinal, pulmonary, and skin diseases. We highlight current advancements in the biology and classification of ILCs in this review. Additionally, we provide a thorough overview of their contributions to several inflammatory bone-related pathologies, including osteoporosis, rheumatoid arthritis, periodontitis, and ankylosing spondylitis. Understanding the multiple functions of ILCs in both physiological and pathological conditions will further mobilize future research towards targeting ILCs for therapeutic purposes.

Extracellular vesicles (EVs), encompassing exosomes, microvesicles (MVs), and apoptotic bodies (ABs), are cell-derived heterogeneous nanoparticles with a pivotal role in intercellular communication. EVs are enclosed by a lipid-bilayer membrane to escape enzymatic degradation. EVs contain various functional molecules (e.g., nucleic acids, proteins, lipids and metabolites) which can be transferred from donor cells to recipient cells. EVs provide many advantages including accessibility, modifiability and easy storage, stability, biocompatibility, heterogeneity and they readily penetrate through biological barriers, making EVs ideal and promising candidates for diagnosis/prognosis biomarkers and therapeutic tools. Recently, EVs were implicated in both physiological and pathophysiological settings of cardiovascular system through regulation of cell-cell communication. Numerous studies have reported a role for EVs in the pathophysiological progression of cardiovascular diseases (CVDs) and have evaluated the utility of EVs for the diagnosis/prognosis and therapeutics of CVDs. In this review, we summarize the biology of EVs, evaluate the perceived biological function of EVs in different CVDs along with a consideration of recent progress for the application of EVs in diagnosis/prognosis and therapies of CVDs.

Myeloid-derived suppressor cells (MDSCs) are important components of the tumor microenvironment (TME), which drive the tumor immune escape by inducing immunosuppression. The expansion and function of MDSCs are tightly associated with signaling pathways induced by molecules from tumor cells, stromal cells, and activated immune cells in the TME. Although these pathways have been well-characterized, the understanding of the epigenetic regulators involved is incomplete. Since histone modifications are the most studied epigenetic changes in MDSCs, we summarize current knowledge on the role of histone modifications in MDSCs within this review. We first discuss the influence of the TME on histone modifications in MDSCs, with an emphasis on histone modifications and modifiers that direct MDSC differentiation and function. Furthermore, we highlight current epigenetic interventions that can reverse MDSC-induced immunosuppression by modulating histone modifications and discuss future research directions to fully appreciate the role of histone modifications in MDSCs.

The Nucleotide-binding domain leucine-rich repeat and pyrin domain containing receptor 3 (NLRP3), a member of the nucleotide-binding oligomerization domain (NOD) like receptors (NLRs) family, plays an important role in the innate immune response against pathogen invasions. NLRP3 inflammasome consisting of NLRP3 protein, the adapter protein apoptosis-associated speck-like protein containing a caspase recruitment domain (CARD) (ASC), and the effector protein pro-caspase-1, is central to this process. Upon activation, NLRP3 inflammasome initiates the release of inflammatory cytokines and triggers a form of cell death known as pyroptosis. Dysregulation or inappropriate activation of NLRP3 has been implicated in various human diseases, including type 2 diabetes, colitis, depression, and gout. Consequently, understanding the mechanism underlying NLRP3 inflammasome activation is critical for the development of therapeutic drugs. In the pursuit of potential therapeutic agents, peptides present several advantages over small molecules. They offer higher selectivity, increased potency, reduced toxicity, and fewer off-target effects. The advancements in molecular biology have expanded the opportunities for applying peptides in medicine, unlocking their vast medical potential. This review begins by providing a comprehensive summary of recent research progress regarding the mechanisms governing NLRP3 inflammasome activation. Subsequently, we offer an overview of current peptide inhibitors capable of modulating the NLRP3 inflammasome activation pathway.

Stroke is one of the devastating clinical conditions that causes death and permanent disability. Its occurrence causes the reduction of oxygen and glucose supply, resulting in events such as inflammatory response, oxidative stress, and apoptosis in the brain. Microglia are brain-resident immune cells in the central nervous system (CNS) that exert diverse roles and respond to pathological process after an ischemic insult. The discovery of fibroblast growth factors (FGFs) in mammals, resulted to the findings that they can treat experimental models of stroke in animals effectively. FGFs function as homeostatic factors that control cells and hormones involved in metabolism, and they also regulate the secretion of proinflammatory (M1) and anti-inflammatory (M2) cytokines after stroke. In this review, we outline current evidence of microglia activation in experimental models of stroke focusing on its ability to exacerbate damage or repair tissue. Also, our review sheds light on the pharmacological actions of FGFs on multiple targets to regulate microglial modulation and highlighted their theoretical molecular mechanisms to provide possible therapeutic targets, as well as their limitations for the treatment of stroke.

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