作者机构：
[Li, Lanfang; Wang, Liwen; Li, LF] Univ South China, Sch Pharm, Inst Pharmaceut Pharmacol, Hengyang 421001, Peoples R China.;[Liu, Huimei] Univ South China, Hengyang Med Sch, Hengyang 421001, Peoples R China.
通讯机构：
[Li, LF ] U;Univ South China, Sch Pharm, Inst Pharmaceut Pharmacol, Hengyang 421001, Peoples R China.
关键词：
p62
摘要：
Neurodegenerative diseases (NDDs), mainly including Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), and Alzheimer's disease (AD), are sporadic and rare genetic disorders of the central nervous system. A key feature of these conditions is the slow accumulation of misfolded protein deposits in brain neurons, the excessive aggregation of which leads to neurotoxicity and further disorders of the nervous system.
摘要：
As an essential trace element for organisms, zinc participates in various physiological processes, such as RNA transcription, DNA replication, cell proliferation, and cell differentiation. The destruction of zinc homeostasis is associated with various diseases. Zinc homeostasis is controlled by the cooperative action of zinc transporter proteins that are responsible for the influx and efflux of zinc. Zinc transporter proteins are mainly categorized into two families: Zrt/Irt-like protein (SLC39A/ZIP) family and zinc transporter (SLC30A/ZNT) family. ZIP transporters contain 14 members, namely ZIP1-14, which can be further divided into four subfamilies. Currently, ZIP transporters-regulated zinc homeostasis is one of the research hotspots. Cumulative evidence suggests that ZIP transporters-regulated zinc homeostasis may cause physiological dysfunction and contribute to the onset and progression of diverse diseases, such as cancers, neurological diseases, and cardiovascular diseases. In this review, we initially discuss the structure and distribution of ZIP transporters. Furthermore, we comprehensively review the latest research progress of ZIP transporters-regulated zinc homeostasis in diseases, providing a new perspective into new therapeutic targets for treating related diseases.
摘要：
The ZDHHC13/ZDHHC17 subfamily belongs to the zinc finger DHHC-domain containing (ZDHHC) family, including ZDHHC13 and ZDHHC17. Recent studies have shown that the ZDHHC13/ZDHHC17 subfamily is involved in various pathological and physiological processes, including S-palmitoylation, Mg(2+) transport, and CALCOCO1-mediated Golgiphagy. Moreover, the ZDHHC13/ZDHHC17 subfamily plays a crucial role in the occurrence and development of many diseases, including Huntington disease (HD), osteoporosis, atopic dermatitis, diabetes, and cancer. In the present review, we describe the distribution, structure, and post-translational modifications (PTMs) of the ZDHHC13/ZDHHC17 subfamily. Moreover, we effectively summarize the biological functions and associated diseases of this subfamily. Given the pleiotropy of the ZDHHC13/ZDHHC17 subfamily, it is imperative to conduct further research on its members to comprehend the pertinent pathophysiological mechanisms and to devise tactics for managing and controlling various diseases.
摘要：
Autophagy is a cellular degradation system that recycles or degrades damaged organelles, viral particles, and aggregated proteins through the lysosomal pathway. Autophagy plays an indispensable role in cellular homeostasis and communication processes. An interesting aspect is that autophagy also mediates the secretion of cellular contents, a process known as secretory autophagy. Secretory autophagy differs from macroautophagy, which sequesters recruited proteins, organelles, or viral particles into autophagosomes and degrades these sequesters in lysosomes, while the secretory autophagy pathway participates in the extracellular export of cellular contents sequestered by autophagosomes through autophagy and endosomal modulators. Recent evidence reveals that secretory autophagy is pivotal in the occurrence and progression of diseases. In this review, we summarize the molecular mechanisms of secretory autophagy. Furthermore, we review the impact of secretory autophagy on diseases, including cancer, viral infectious diseases, neurodegenerative diseases, and cardiovascular diseases. Considering the pleiotropic actions of secretory autophagy on diseases, studying the mechanism of secretory autophagy may help to understand the relevant pathophysiological processes.
摘要：
A wealth of research indicates that superficial gastritis (SG) and atrophic gastritis (AG) are precursors to gastric cancer (GC). While Helicobacter pylori (H. pylori) has long been recognized as a key player in GC development, recent findings by Fu et al. have identified Streptococcus anginosus (S. anginosus) as an emerging pathogen that can trigger SG, AG and GC. S. anginosus, a gram-positive coccus, leverages its surface protein T. pallidum membrane protein C (TMPC) to engage with the annexin A2 (ANXA2) receptor of gastric epithelial cells, facilitating its colonization and invasion in the gastric mucosa. This leads to an upregulation of proinflammatory chemokines Ccl20 and Ccl8, causing prolonged effects on gastric barrier function and microbiota homeostasis, leading to SG. Moreover, these bacteria activate the mitogen-activated protein kinase (MAPK) signaling pathway, which is associated with the development of AG and GC. Importantly, inhibiting TMPC or knocking down ANXA2 can reduce S. anginosus colonization and invasion, lowering the chances of SG, AG, and GC. This paper highlights the molecular mechanisms of S. anginosus in SG, AG and GC, emphasizing the importance of a multi-pathogen strategy in gastric disease management and the need for further investigation into the role of S. anginosus in GC progression.
摘要：
Mitochondria, the dynamic organelles responsible for energy production and cellular metabolism, have the metabolic function of extracting energy from nutrients and synthesizing crucial metabolites. Nevertheless, recent research unveils that intercellular mitochondrial transfer by tunneling nanotubes, tumor microtubes, gap junction intercellular communication, extracellular vesicles, endocytosis and cell fusion may regulate mitochondrial function within recipient cells, potentially contributing to disease treatment, such as nonalcoholic steatohepatitis, glioblastoma, ischemic stroke, bladder cancer and neurodegenerative diseases. This review introduces the principal approaches to intercellular mitochondrial transfer and examines its role in various diseases. Furthermore, we provide a comprehensive overview of the inhibitors and activators of intercellular mitochondrial transfer, offering a unique perspective to illustrate the relationship between intercellular mitochondrial transfer and diseases. Relationship between mitochondrial transfer mediated by different pathways and diseasesimage
通讯机构：
[Linxi Chen; Lanfang Li] I;Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, 421001, Hunan, China
摘要：
Glycometabolism is well known for its roles as the main source of energy, which mainly includes three metabolic pathways: oxidative phosphorylation, glycolysis and pentose phosphate pathway. The orderly progress of glycometabolism is the basis for the maintenance of cardiovascular function. However, upon exposure to harmful stimuli, the intracellular glycometabolism changes or tends to shift toward another glycometabolism pathway more suitable for its own development and adaptation. This shift away from the normal glycometabolism is also known as glycometabolism reprogramming, which is commonly related to the occurrence and aggravation of cardiovascular diseases. In this review, we elucidate the physiological role of glycometabolism in the cardiovascular system and summarize the mechanisms by which glycometabolism drives cardiovascular diseases, including diabetes, cardiac hypertrophy, heart failure, atherosclerosis, and pulmonary hypertension. Collectively, directing GMR back to normal glycometabolism might provide a therapeutic strategy for the prevention and treatment of related cardiovascular diseases.
作者机构：
[Liu, Huimei; Fan, Sisi; Li, Lanfang] Univ South China, Inst Pharm & Pharmacol, Hunan Prov Cooperat Innovat Ctr Mol Target New Dru, Hengyang Med Sch,Hunan Prov Key Lab Tumor Microenv, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Li, Lanfang] I;Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of tumor microenvironment responsive drug research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China. Electronic address:
关键词：
chemokine receptor CXCR1;chemokine receptor CXCR2;clathrin;cyclic GMP;fat droplet;G protein coupled receptor;neural retinal leucine zipper protein;protein;receptor expression enhancing protein 1;receptor expression enhancing protein 2;receptor expression enhancing protein 3;receptor expression enhancing protein 4;receptor expression enhancing protein 5;receptor expression enhancing protein 6;transcription factor;unclassified drug;carrier protein;G protein coupled receptor;REEP1 protein, human;REEP4 protein, human;adipose tissue;Alzheimer disease;aneuploidy;atrial fibrillation;autism;bioenergy;biogenesis;bioinformatics;blepharospasm;breast cancer;cell nucleus membrane;cell structure;depression;diabetes mellitus;disease control;disease course;gene regulatory network;heart failure;hereditary motor sensory neuropathy;homeostasis;human;lipid metabolism;liver cell carcinoma;malignant neoplasm;Meige syndrome;microtubule;morphogenesis;nonhuman;obsessive compulsive disorder;Parkinson disease;pathophysiology;phylogeny;protein expression;protein function;protein localization;protein structure;retina disease;Review;sarcoplasmic reticulum;signal transduction;sperm function;systemic juvenile idiopathic arthritis;tissue differentiation;vesicle trafficking;cytoskeleton;endoplasmic reticulum;metabolism;Carrier Proteins;COVID-19;Cytoskeleton;Endoplasmic Reticulum;Humans;Membrane Transport Proteins;Receptors, G-Protein-Coupled
作者机构：
[Ouyang X.; Chen L.; Chen W.; Li L.] Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, 421001, China
通讯机构：
[Chen, L.; Li, L.] I;Institute of Pharmacy and Pharmacology, China
摘要：
Endoplasmic reticulum(ER)is the largest organelle in eukaryotic cells, which can participate in the maintenance of calcium(Ca~(2+))homeostasis, protein synthesis and organelle communication[1]. Endoplasmic reticulum autophagy(ER-phagy)is a cellular quality control pathway mediated by autophagy receptors. ER-phagy involves the engulfing of excess or misfolded proteins and superfluous ER membrane to form autophagosomes which are degraded by lysosome[1]. ER-phagy occurs under normal conditions and is enhanced during starvation. At present, the receptors of ER-phagy in mammalian cells include family sequence similarity 134[1], membrane B(FAM134B), SEC62, reticulin 3(RTN3), cell cycle progression 1(CCPG1), atlastin GTPase 3(ATL3), testis expressed gene 264(TEX264), tripartite motif containing 13(TRIM13, also known as RFP2), and coiled-coil domain protein 1(CALCOCO1)[2]. FAM134B is recognized as the most characteristic receptor for ER-phagy in mammalian cells[1]. FAM134B consists of a reticulonhomology domain(RHD), a C-terminal cytoplasmic domain and an N-terminal cytoplasmic domain[1]. The RHD region of FAM134B senses and induces ER membrane curvature for ER-phagy. The LC3-interacting region(LIR), located in the C-terminal cytoplasmic domain of FAM134B, is responsible for recruiting and binding the autophagy modifiers LC3 and GABARAP, which involves the engulfing of degradable cargo to phagophore membranes for ER-phagy[1,3]. FAM134B plays a critical role in ER function and quality control through mediating ER-phagy. Inhibition of FAM134B expression leads to ER expansion. Contrarily, up-regulation of FAM134B level results in ER fragmentation[1].
作者机构：
[Chen L.; Li L.; Fan S.; Chen W.] Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, 421001, China
通讯机构：
[Chen, L.; Li, L.] I;Institute of Pharmacy and Pharmacology, China
关键词：
DRUGS;ORGANS;TREATMENT
摘要：
Fibrosis, the self-repair process of the body after tissue damage, is a common pathological feature of many chronic inflammatory diseases. It occurs in a variety of organs, leading to structural destruction and hypofunction, and even organ failure. Fibrosis in organ tissues is characterized by chronic inflammation, excessive accumulation of extracellular matrix (ECM) components, and the decrease of parenchymal cells. Fibrosis is caused by persistent infections, toxins, autoimmune diseases, radiation, and mechanical injury. To date, there are various therapeutic strategies for organ fibrosis, such as changing lifestyle, using antiviral drugs, anti-in-flammatory treatment, using interferon, and organ transplantation. Currently, there are only two FDA-approved drugs for the treatment of idiopathic pulmonary fibrosis (IPF), i.e., pirfenidone and nintedanib. Nevertheless, the mechanisms of action of these drugs are not fully understood, the cost is high, and there is no way to prevent or reverse the disease process. Consequently, it is extremely important for us to better understand the pathogenesis of fibrosis, strengthen the screening and evaluation of new drugs, and improve the existing drugs. And it can also help us to treat and prevent fibrosis in the future.
通讯机构：
[Linxi Chen; Lanfang Li] H;Hunan Provincial Key Laboratory of tumor microenvironment responsive drug research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Institute of Pharmacy and Pharmacology, University of South China, Hengyang, Hunan, China
作者机构：
[Liu, Huimei; Zhu, Li; Li, Lanfang; Chen, Linxi] Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hunan Prov Key Lab Tumor Microenvironm Respons Dr, Inst Pharm & Pharmacol,Hengyang Med Sch, Hengyang, Hunan, Peoples R China.
通讯机构：
[Linxi Chen; Lanfang Li] I;Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of tumor microenvironment responsive drug research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang Medical School, University of South China, Hengyang, Hunan, China
关键词：
antiinflammation;atherosclerosis;cholesterol;macrophage;traditional Chinese medicine
摘要：
Atherosclerosis is the onset of endothelial cell damage and is characterized by abnormal accumulation of fibrinogen and lipid in large and middle arteries. Recent researches indicate that traditional Chinese medicine including Notoginseng Radix et Rhizoma, Astragali Radix, Salviae Miltiorrhizae Radix et Rhizoma, Ginseng Radix et Rhizoma, Fructus Crataegi, Glycyrrhizae Radix et Rhizoma, Polygoni Multiflori Radix, Fructus Lycii, and Coptidis Rhizoma have therapeutic effects on atherosclerosis. Furthermore, the pharmacological roles of these kinds of traditional Chinese medicine in atherosclerosis refer to endothelial function influences, cell proliferation and migration, platelet aggregation, thrombus formation, oxidative stress, inflammation, angiogenesis, apoptosis, autophagy, lipid metabolism, and the gut microbiome. Traditional Chinese medicine may serve as potential and effective anti-atherosclerosis drugs. However, a critical study has shown that Notoginseng Radix et Rhizoma may also have toxic effects including pustules, fever, and elevate circulating neutrophil count. Further high-quality studies are still required to determine the clinical safety and efficacy of traditional Chinese medicine and its active ingredients.
