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1.
The Ion Channels of Endomembranes.
Hu, M, Feng, X, Liu, Q, Liu, S, Huang, F, Xu, H
Physiological reviews. 2024
Abstract
The endomembrane system consists of organellar membranes in the biosynthetic pathway: endoplasmic reticulum (ER), Golgi apparatus, and secretory vesicles, as well as those in the degradative pathway: early endosomes, macropinosomes, phagosomes, autophagosomes, late endosomes, and lysosomes. These endomembrane organelles/vesicles work together to synthesize, modify, package, transport, and degrade proteins, carbohydrates, and lipids, regulating the balance between cellular anabolism and catabolism. Large ion concentration gradients exist across endomembranes - Ca2+ gradients for most endomembrane organelles and H+ gradients for the acidic compartments. Ion (Na+, K+, H+, Ca2+, and Cl-) channels on the organellar membranes control ion flux in response to cellular cues, allowing rapid informational exchange between the cytosol and organelle lumen. Recent advances in organelle proteomics, organellar electrophysiology, luminal and juxta-organellar ion imaging have led to molecular identification and functional characterization of about two dozen endomembrane ion channels. For example, whereas IP3R1-3 channels mediate Ca2+ release from the ER in response to neurotransmitter and hormone stimulation, TRPML1-3 and TMEM175 channels mediate lysosomal Ca2+ and H+ release, respectively, in response to nutritional and trafficking cues. This review aims to summarize the current understandings of these endomembrane channels, with a focus on their subcellular localizations, ion permeation properties, gating mechanisms, cell biological functions, and disease relevance.
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2.
Interventions for the detection, monitoring, and management of chronic non-communicable diseases in the prison population: an international systematic review.
Hewson, T, Minchin, M, Lee, K, Liu, S, Wong, E, Edge, C, Hard, J, Forsyth, K, Senior, J, Shaw, J
BMC public health. 2024;(1):292
Abstract
BACKGROUND High rates of health inequalities and chronic non-communicable diseases exist amongst the prison population. This places people in and/or released from prison at heightened risk of multimorbidity, premature mortality, and reduced quality of life. Ensuring appropriate healthcare for people in prison to improve their health outcomes is an important aspect of social justice. This review examines the global literature on healthcare interventions to detect, monitor and manage chronic non-communicable diseases amongst the prison population and people recently released from prison. METHODS Systematic searches of EMBASE, MEDLINE, CINAHL, Web of Science, Scopus, and the Cochrane Library were conducted and supplemented by citation searching and review of the grey literature. The literature searches attempted to identify all articles describing any healthcare intervention for adults in prison, or released from prison in the past 1 year, to detect, monitor, or manage any chronic non-communicable illness. 19,061 articles were identified, of which 1058 articles were screened by abstract and 203 articles were reviewed by full text. RESULTS Sixty-five studies were included in the review, involving 18,311 participants from multiple countries. Most studies were quasi-experimental and/or low to moderate in quality. Numerous healthcare interventions were described in the literature including chronic disease screening, telemedicine, health education, integrated care systems, implementing specialist equipment and staff roles to manage chronic diseases in prisons, and providing enhanced primary care contact and/or support from community health workers for people recently released from prison. These interventions were associated with improvement in various measures of clinical and cost effectiveness, although comparison between different care models was not possible due to high levels of clinical heterogeneity. CONCLUSIONS It is currently unclear which interventions are most effective at monitoring and managing chronic non-communicable diseases in prison. More research is needed to determine the most effective interventions for improving chronic disease management in prisons and how these should be implemented to ensure optimal success. Future research should examine interventions for addressing multimorbidity within prisons, since most studies tested interventions for a singular non-communicable disease.
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3.
The role of zinc finger proteins in the fate determination of mesenchymal stem cells during osteogenic and adipogenic differentiation.
Li, B, Liu, S, He, Z, Luo, E, Liu, H
The international journal of biochemistry & cell biology. 2024;:106507
Abstract
Zinc finger proteins (ZFPs) constitute a crucial group of transcription factors widely present in various organisms. They act as transcription factors, nucleases, and RNA-binding proteins, playing significant roles in cell differentiation, growth, and development. With extensive research on ZFPs, their roles in the determination of mesenchymal stem cells (MSCs) fate during osteogenic and adipogenic differentiation processes have become increasingly clear. ZFP521, for instance, is identified as an inhibitor of the Wnt signaling pathway and RUNX2's transcriptional activity, effectively suppressing osteogenic differentiation. Moreover, ZFP217 contributes to the inhibition of adipogenic differentiation by reducing the M6A level of the cell cycle regulator cyclin D1 (CCND1). In addition, other ZFPs can also influence the fate of mesenchymal stem cells (MSCs) during osteogenic and adipogenic differentiation through various signaling pathways, transcription factors, and epigenetic controls, participating in the subsequent differentiation and maturation of precursor cells. Given the prevalent occurrence of osteoporosis, obesity, and related metabolic disorders, a comprehensive understanding of the regulatory mechanisms balancing bone and fat metabolism is essential, with a particular focus on the fate determination of MSCs in osteogenic and adipogenic differentiation. In this review, we provide a detailed summary of how zinc finger proteins influence the osteogenic and adipogenic differentiation of MSCs through different signaling pathways, transcription factors, and epigenetic mechanisms. Additionally, we outline the regulatory mechanisms of ZFPs in controlling osteogenic and adipogenic differentiation based on various stages of MSC differentiation.
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4.
Targeting EBV-encoded products: Implications for drug development in EBV-associated diseases.
Lv, M, Ding, Y, Zhang, Y, Liu, S
Reviews in medical virology. 2024;(1):e2487
Abstract
Epstein-Barr virus, a human gamma-herpesvirus, has a close connection to the pathogenesis of cancers and other diseases, which are a burden for public health worldwide. So far, several drugs or biomolecules have been discovered that can target EBV-encoded products for treatment, such as Silvestrol, affinity toxin, roscovitine, H20, H31, curcumin, thymoquinone, and ribosomal protein L22. These drugs activate or inhibit the function of some biomolecules, affecting subsequent signalling pathways by acting on the products of EBV. These drugs usually target LMP1, LMP2; EBNA1, EBNA2, EBNA3; EBER1, EBER2; Bam-HI A rightward transcript and BHRF1. Additionally, some promising findings in the fields of vaccines, immunological, and cellular therapies have been established. In this review, we mainly summarise the function of drugs mentioned above and unique mechanisms, hoping that we can help giving insight to the design of drugs for the treatment of EBV-associated diseases.
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5.
Exploring the relationship between hyperlactatemia and anemia.
Zhang, S, Liu, W, Ganz, T, Liu, S
Trends in endocrinology and metabolism: TEM. 2024
Abstract
Hyperlactatemia and anemia commonly coexist and their crosstalk is a longstanding mystery with elusive mechanisms involved in physical activities, infections, cancers, and genetic disorders. For instance, hyperlactatemia leads to iron restriction by upregulating hepatic hepcidin expression. Increasing evidence also points to lactate as a crucial signaling molecule rather than merely a metabolic byproduct. Here, we discuss the mutual influence between anemia and hyperlactatemia. This opinion calls for a reconsideration of the multifaceted roles of lactate and lactylation in anemia and emphasizes the need to fill knowledge gaps, including the dose dependence of lactate's effects, its sources, and its subcellular localization.
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6.
Epigenetic modifications in obesity-associated diseases.
Long, Y, Mao, C, Liu, S, Tao, Y, Xiao, D
MedComm. 2024;(2):e496
Abstract
The global prevalence of obesity has reached epidemic levels, significantly elevating the susceptibility to various cardiometabolic conditions and certain types of cancer. In addition to causing metabolic abnormalities such as insulin resistance (IR), elevated blood glucose and lipids, and ectopic fat deposition, obesity can also damage pancreatic islet cells, endothelial cells, and cardiomyocytes through chronic inflammation, and even promote the development of a microenvironment conducive to cancer initiation. Improper dietary habits and lack of physical exercise are important behavioral factors that increase the risk of obesity, which can affect gene expression through epigenetic modifications. Epigenetic alterations can occur in early stage of obesity, some of which are reversible, while others persist over time and lead to obesity-related complications. Therefore, the dynamic adjustability of epigenetic modifications can be leveraged to reverse the development of obesity-associated diseases through behavioral interventions, drugs, and bariatric surgery. This review provides a comprehensive summary of the impact of epigenetic regulation on the initiation and development of obesity-associated cancers, type 2 diabetes, and cardiovascular diseases, establishing a theoretical basis for prevention, diagnosis, and treatment of these conditions.
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7.
Advanced postoperative tissue antiadhesive membranes enabled with electrospun nanofibers.
Zhu, Y, Zhang, C, Liang, Y, Shi, J, Yu, Q, Liu, S, Yu, D, Liu, H
Biomaterials science. 2024
Abstract
Tissue adhesion is one of the most common postoperative complications, which is frequently accompanied by inflammation, pain, and even dyskinesia, significantly reducing the quality of life of patients. Thus, to prevent the formation of tissue adhesions, various strategies have been explored. Among these methods, placing anti-adhesion membranes over the injured site to separate the wound from surrounding tissues is a simple and prominently favored method. Recently, electrospun nanofibers have been the most frequently investigated antiadhesive membranes due to their tunable porous structure and high porosities. They not only can act as an essential barrier and functional carrier system but also allow for high permeability and nutrient transport, showing great potential for preventing tissue adhesion. Herein, we provide a short review of the most recent applications of electrospun nanofibrous antiadhesive membranes in tendons, the abdominal cavity, dural sac, pericardium, and meninges. Firstly, each section highlights the most representative examples and they are sorted based on the latest progress of related research. Moreover, the design principles, preparation strategies, overall performances, and existing problems are highlighted and evaluated. Finally, the current challenges and several future ways to develop electrospun nanofibrous antiadhesive membranes are proposed. The systematic discussion and proposed directions can shed light on ideas and guide the reasonable design of electrospun nanofibrous membranes, contributing to the development of exceptional tissue anti-adhesive materials in the foreseeable future.
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8.
Dual-directional regulation of spinal cord injury and the gut microbiota.
Cui, Y, Liu, J, Lei, X, Liu, S, Chen, H, Wei, Z, Li, H, Yang, Y, Zheng, C, Li, Z
Neural regeneration research. 2024;(3):548-556
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Abstract
There is increasing evidence that the gut microbiota affects the incidence and progression of central nervous system diseases via the brain-gut axis. The spinal cord is a vital important part of the central nervous system; however, the underlying association between spinal cord injury and gut interactions remains unknown. Recent studies suggest that patients with spinal cord injury frequently experience intestinal dysfunction and gut dysbiosis. Alterations in the gut microbiota can cause disruption in the intestinal barrier and trigger neurogenic inflammatory responses which may impede recovery after spinal cord injury. This review summarizes existing clinical and basic research on the relationship between the gut microbiota and spinal cord injury. Our research identified three key points. First, the gut microbiota in patients with spinal cord injury presents a key characteristic and gut dysbiosis may profoundly influence multiple organs and systems in patients with spinal cord injury. Second, following spinal cord injury, weakened intestinal peristalsis, prolonged intestinal transport time, and immune dysfunction of the intestine caused by abnormal autonomic nerve function, as well as frequent antibiotic treatment, may induce gut dysbiosis. Third, the gut microbiota and associated metabolites may act on central neurons and affect recovery after spinal cord injury; cytokines and the Toll-like receptor ligand pathways have been identified as crucial mechanisms in the communication between the gut microbiota and central nervous system. Fecal microbiota transplantation, probiotics, dietary interventions, and other therapies have been shown to serve a neuroprotective role in spinal cord injury by modulating the gut microbiota. Therapies targeting the gut microbiota or associated metabolites are a promising approach to promote functional recovery and improve the complications of spinal cord injury.
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A narrative review of the role of HDAC6 in idiopathic pulmonary fibrosis.
Yu, H, Liu, S, Wang, S, Gu, X
Journal of thoracic disease. 2024;(1):688-695
Abstract
BACKGROUND AND OBJECTIVE Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible condition characterized by the deposition of extracellular matrix resulting from repetitive damage to the alveolar epithelium. These injuries, along with dysregulated wound repair and fibroblast dysfunction, lead to continuous tissue remodeling and fibrosis, eventually resulting in end-stage pulmonary fibrosis. Currently, there is no specific pharmacological treatment available for IPF. The role of inflammation in the development of IPF is still a topic of debate, and it is sometimes considered incidental to fibrosis. Over the past decade, macrophages have emerged as significant contributors to the pathogenesis of fibrosis. M1 macrophages are responsible for wound healing following alveolar epithelial injury, while M2 macrophages are involved in resolving wound repair and terminating the inflammatory response in the lungs. Various studies provide evidence that M2-like macrophages contribute to the abnormal fibrogenesis. In recent years, there has been growing interest in understanding macrophage polarization and its role in the development of pulmonary fibrosis. Histone deacetylase 6 (HDAC6), a member of the HDAC family with two functional deacetylase structural domains and a ubiquitin-binding zinc finger structural domain (ZnF-BUZ), plays a crucial role in pulmonary fibrosis. This article explores the role of HDAC6 in pulmonary fibrosis and evaluates its potential as a treatment approach for IPF. METHODS PubMed, Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang, China Biomedical Literature Service System (CBMdisc) and Web of Science were searched to obtain researches, published in English and Chinese, until July 2023. The search was performed using specific keywords such as Histone deacetylase 6, HDAC6, Idiopathic pulmonary fibrosis, IPF, fibrosis. KEY CONTENT AND FINDINGS HDAC6 has diverse effects on physiological processes, including the NLRP3 inflammasome, epithelial-mesenchymal transition, the TGFβ-PI3K-AKT pathway, macrophage polarization and TGF-β-Smad signaling pathway, due to its unique structure. HDAC6 has been found to enhance the inflammatory response and fibrosis of lung tissues, contributing to the development of IPF. CONCLUSIONS In the future, HDAC6 inhibitors are expected to play a crucial role in the treatment of fibrotic disorders and should be studied further deserves to pursue in future research.
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10.
Potential Therapeutic Effects of Short-Chain Fatty Acids on Chronic Pain.
Tang, Y, Du, J, Wu, H, Wang, M, Liu, S, Tao, F
Current neuropharmacology. 2024;(2):191-203
Abstract
The intestinal homeostasis maintained by the gut microbiome and relevant metabolites is essential for health, and its disturbance leads to various intestinal or extraintestinal diseases. Recent studies suggest that gut microbiome-derived metabolites short-chain fatty acids (SCFAs) are involved in different neurological disorders (such as chronic pain). SCFAs are produced by bacterial fermentation of dietary fibers in the gut and contribute to multiple host processes, including gastrointestinal regulation, cardiovascular modulation, and neuroendocrine-immune homeostasis. Although SCFAs have been implicated in the modulation of chronic pain, the detailed mechanisms that underlie such roles of SCFAs remain to be further investigated. In this review, we summarize currently available research data regarding SCFAs as a potential therapeutic target for chronic pain treatment and discuss several possible mechanisms by which SCFAs modulate chronic pain.