17 results on '"Pang, Qiwen"'
Search Results
2. Gut microbiota: A magical multifunctional target regulated by medicine food homology species
- Author
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Zuo, Wei-Fang, Pang, Qiwen, Yao, Lai-Ping, Zhang, Yang, Peng, Cheng, Huang, Wei, and Han, Bo
- Published
- 2023
- Full Text
- View/download PDF
3. RAGE/galectin-3 yields intraplaque calcification transformation via sortilin
- Author
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Sun, Zhen, Wang, Zhongqun, Li, Lihua, Yan, Jinchuan, Shao, Chen, Bao, Zhengyang, Jing, Lele, Pang, Qiwen, Geng, Yue, and Zhang, Lili
- Published
- 2019
- Full Text
- View/download PDF
4. Lighting the way to diverse cyclic architectures: expanding the horizons with photogenerated ketenes in sustainable chemistry
- Author
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Zuo, Wei-Fang, Liu, Qian, Xie, Xin, Pang, Qiwen, Li, Wei, Peng, Cheng, Li, Xiang, and Han, Bo
- Abstract
Light is a fundamental energy source that has considerably driven scientific progress, especially in the fields of synthetic chemistry and pharmaceuticals. Visible-light-mediated synthetic chemistry has revolutionized conventional bond formation and enabled previously inaccessible chemical processes under mild conditions. However, the continuous consumption of photocatalysts and corresponding additives has led to system complexity and cost escalation, making the development of photoactivated substrates a promising yet challenging research frontier. Recently, the emerging photogenerated ketenes as a potent class of organic compounds has provided a promising solution to the challenges associated with classic ketene preparation and application, with reduced preparative costs and simplified processes. This review highlights how photogenerated ketenes have simplified and accelerated the synthesis of diverse cyclic architectures through [2 + n] cyclization reactions and complex natural products through Danheiser benzannulation. Significantly, their successful application in flow chemistry has demonstrated remarkable potential for industrialization. Despite challenges in terms of limited cyclic architectures, elusive mechanisms, and challenging chiral control, ongoing efforts investigating the chemical behaviors of photogenerated ketenes and exploring their potential applications hold promise for breakthrough discoveries possible, propelling the field forward sustainable.
- Published
- 2023
5. Role of Matrix Vesicles in Bone–Vascular Cross-Talk
- Author
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Jing, Lele, Li, Lihua, Sun, Zhen, Bao, Zhengyang, Shao, Chen, Yan, Jinchuan, Pang, Qiwen, Geng, Yue, Zhang, Lili, Wang, Xiaodong, and Wang, Zhongqun
- Published
- 2019
- Full Text
- View/download PDF
6. Assembly of spirocyclic pyrazolone-pyrrolo[4,3,2-de]quinoline skeleton via cascade [1,5] hydride transfer/cyclization by C(sp3)–H functionalization.
- Author
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Xie, Xin, Huang, He, Fan, Yu, Luo, Yuan, Pang, Qiwen, Li, Xiang, and Huang, Wei
- Published
- 2023
- Full Text
- View/download PDF
7. Recent Advances on Direct Functionalization of Indoles in Aqueous Media.
- Author
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Pang, Qiwen, Zuo, Wei‐Fang, Zhang, Yang, Li, Xiang, and Han, Bo
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CHEMICAL processes , *INDOLE compounds , *INDOLE derivatives , *SUSTAINABLE chemistry , *HETEROCYCLIC compounds , *INDOLE - Abstract
Indoles and their derivatives have dominated a significant proportion of nitrogen‐containing heterocyclic compounds and play an essential role in synthetic and medicinal chemistry, pesticides, and advanced materials. Compared with conventional synthetic strategies, direct functionalization of indoles provides straightforward access to construct diverse indole scaffolds. As we enter an era emphasizing green and sustainable chemistry, utilizing environment‐friendly solvents represented by water demonstrates great potential in synthesizing valuable indole derivatives. This review aims to depict the critical aspects of aqueous‐mediated indoles functionalization over the past decade and discusses the future challenges and prospects in this fast‐growing field. For the convenience of readers, this review is classified into three parts according to the bonding modes (C−C, C−N, and C−S bonds), which focus on the diversity of indole derivatives, the prominent role of water in the chemical process, and the types of catalyst systems and mechanisms. We hope this review can promote the sustainable development of the direct functionalization of indoles and their derivatives and the discovery of novel and practical organic methods in aqueous phase. [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
- View/download PDF
8. Advanced Glycation End Products Induce Vascular Smooth Muscle Cell-Derived Foam Cell Formation and Transdifferentiate to a Macrophage-Like State.
- Author
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Bao, Zhengyang, Li, Lihua, Geng, Yue, Yan, Jinchuan, Dai, Zhiyin, Shao, Chen, Sun, Zhen, Jing, Lele, Pang, Qiwen, Zhang, Lili, Wang, Xiaodong, and Wang, Zhongqun
- Subjects
ADVANCED glycation end-products ,VASCULAR smooth muscle ,ENZYME-linked immunosorbent assay ,PEOPLE with diabetes ,ATHEROSCLEROTIC plaque - Abstract
Background. Advanced glycation end products play an important role in diabetic atherosclerosis. The effects of advanced glycation end products (AGEs) on vascular smooth muscle cell- (VSMC-) derived foam cell formation and phenotypic transformation are unknown. Methods. Serological and histological samples were obtained from diabetic amputation patients and accident amputation patients from the Affiliated Hospital of Jiangsu University. CD68/Actin Alpha 2 (ACTA2) coimmunofluorescence sections were used to quantify the number of VSMCs with macrophage-like phenotypes. Western blotting was used to detect the expression of the receptor of advanced glycation end products in vascular samples. Enzyme-linked immunosorbent assay (ELISA) was used to evaluate the level of serum Nε-carboxymethyl-lysine (CML). In vitro oil red O staining was used to examine lipid accumulation in VSMCs stimulated by CML. The expression of VSMCs and macrophage markers was measured by western blotting and quantitative real-time PCR. Furthermore, changes in VSMC migration and secretion were detected by the Transwell assay and ELISA. Results. In the arterial plaque sections of diabetic patients, VSMCs transformed to a macrophage-like phenotype. The serum CML and RAGE levels in the plaques were significantly higher in the diabetes group than those in the healthy control group and were significantly related to the number of macrophage-like VSMCs. CML stimulation promoted intracellular lipid accumulation. However, CML stimulation decreased the expression of VSMC markers and increased the expression of macrophage phenotype markers. Finally, CML promoted smooth muscle cell migration and the secretion of proinflammatory-related factors. Conclusions. CML induces VSMC-derived foam cell formation, and VSMCs transdifferentiate to a macrophage-like state, which may be mediated by the activation of RAGE. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
9. N -Carboxymethyl-Lysine Negatively Regulates Foam Cell Migration via the Vav1/Rac1 Pathway.
- Author
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Bao, Zhengyang, Zhang, Lili, Li, Lihua, Yan, Jinchuan, Pang, Qiwen, Sun, Zhen, Geng, Yue, Jing, Lele, Shao, Chen, and Wang, Zhongqun
- Subjects
CELL migration ,ADVANCED glycation end-products ,RECEPTOR for advanced glycation end products (RAGE) ,FOAM cells ,PERITONEAL macrophages ,DIABETIC foot ,ATHEROSCLEROTIC plaque - Abstract
Background: Macrophage-derived foam cells play a central role in atherosclerosis, and their ultimate fate includes apoptosis, promotion of vascular inflammation, or migration to other tissues. Nε-Carboxymethyl-lysine (CML), the key active component of advanced glycation end products, induced foam cell formation and apoptosis. Previous studies have shown that the Vav1/Rac1 pathway affects the macrophage cytoskeleton and cell migration, but its role in the pathogenesis of diabetic atherosclerosis is unknown.Methods and Results: In this study, we used anterior tibiofibular vascular samples from diabetic foot amputation patients and accident amputation patients, and histological and cytological tests were performed using a diabetic ApoE-/- mouse model and primary peritoneal macrophages, respectively. The results showed that the atherosclerotic plaques of diabetic foot amputation patients and diabetic ApoE-/- mice were larger than those of the control group. Inhibition of the Vav1/Rac1 pathway reduced vascular plaques and promoted the migration of macrophages to lymph nodes. Transwell and wound healing assays showed that the migratory ability of macrophage-derived foam cells was inhibited by CML. Cytoskeletal staining showed that advanced glycation end products inhibited the formation of lamellipodia in foam cells, and inhibition of the Vav1/Rac1 pathway restored the formation of lamellipodia.Conclusion: CML inhibits the migration of foam cells from blood vessels via the Vav1/Rac1 pathway, and this process affects the formation of lamellipodia. [ABSTRACT FROM AUTHOR]- Published
- 2020
- Full Text
- View/download PDF
10. Mechanisms of Matrix Vesicles Mediating Calcification Transition in Diabetic Plaque.
- Author
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Wang, Zhongqun, Zhang, Lili, Sun, Zhen, Shao, Chen, Li, Yukun, Bao, Zhengyang, Jing, Lele, Geng, Yue, Gu, Wen, Pang, Qiwen, Li, Lihua, and Yan, Jinchuan
- Subjects
- *
CALCIFICATION , *ADVANCED glycation end-products , *ANIMAL experimentation , *ATHEROSCLEROSIS , *CALCINOSIS , *EXTRACELLULAR space , *DIABETIC angiopathies - Abstract
Vascular calcification is a key character of advanced plaque in diabetic atherosclerosis. Microcalcification induces plaque rupture, whereas macrocalcification contributes to plaque stability. However, there is still no clear explanation for the formation and transition of these two types of calcification. Based on existing work and the latest international progress, this article provides a brief review of four aspects: calcification transition in plaque; matrix vesicle-mediated calcification transition in plaque; regulation mechanism of matrix vesicle-mediated calcification transition in diabetic plaque; and proposal of a new hypothesis, which may offer a new perspective on the study of the mechanism of calcification transition in plaque. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
11. Assembly of spirocyclic pyrazolone-pyrrolo[4,3,2- de ]quinoline skeleton via cascade [1,5] hydride transfer/cyclization by C(sp 3 )-H functionalization.
- Author
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Xie X, Huang H, Fan Y, Luo Y, Pang Q, Li X, and Huang W
- Abstract
Herein, a highly efficient, scalable, and cascade [1,5] hydride transfer/cyclization method for constructing unique spirocyclic pyrazolone-pyrrolo[4,3,2- de ]quinoline structures via C(sp
3 )-H functionalization is achieved, using pyrazolones and oxindoles attached to C4 amines. This strategy represents a limited approach utilizing C-H activation to construct spirocyclic pyrazolone scaffolds with moderate to excellent reaction performance.- Published
- 2023
- Full Text
- View/download PDF
12. Application of Novel Degraders Employing Autophagy for Expediting Medicinal Research.
- Author
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Li X, Liu Q, Xie X, Peng C, Pang Q, Liu B, and Han B
- Subjects
- Humans, Autophagosomes metabolism, Proteolysis, Autophagy, Neurodegenerative Diseases drug therapy, Neurodegenerative Diseases metabolism
- Abstract
Targeted protein degradation (TPD) technology is based on a unique pharmacological mechanism that has profoundly revolutionized medicinal research by overcoming limitations associated with traditional small-molecule drugs. Autophagy, a mechanism for intracellular waste disposal and recovery, is an important biological process in medicinal research. Recently, studies have demonstrated that several emerging autophagic degraders can treat human diseases. Herein we summarize the progress in medicinal research on autophagic degraders, including autophagosome-tethering compounds (ATTEC), autophagy-targeting chimeras (AUTAC), and AUTOphagy-TArgeting chimeras (AUTOTAC), for treating human diseases. These autophagic degraders exhibit excellent potential for treating neurodegenerative diseases. Our research on autophagic degraders provides a new avenue for medicinal research on TPD via autophagy.
- Published
- 2023
- Full Text
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13. The emerging role of radical chemistry in the amination transformation of highly strained [1.1.1]propellane: Bicyclo[1.1.1]pentylamine as bioisosteres of anilines.
- Author
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Pang Q, Li Y, Xie X, Tang J, Liu Q, Peng C, Li X, and Han B
- Abstract
Bicyclo[1.1.1]pentylamines (BPCAs), emerging as sp
3 -rich surrogates for aniline and its derivatives, demonstrate unique structural features and physicochemical profiles in medicinal and synthetic chemistry. In recent years, compared with conventional synthetic approaches, the rapid development of radical chemistry enables the assembly of valuable bicyclo[1.1.1]pentylamines scaffold directly through the amination transformation of highly strained [1.1.1]propellane. In this review, we concisely summarize the emerging role of radical chemistry in the construction of BCPAs motif, highlighting two different and powerful radical-involved strategies including C -centered and N -centered radical pathways under appropriate conditions. The future direction concerning BCPAs is also discussed at the end of this review, which aims to provide some inspiration for the research of this promising project., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Pang, Li, Xie, Tang, Liu, Peng, Li and Han.)- Published
- 2022
- Full Text
- View/download PDF
14. Construction of Oxo-Bridged Diazocines via Rhodium-Catalyzed (4+3) Cycloaddition of Carbonyl Ylides with Azoalkenes.
- Author
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Pang Q, Zhou J, Wu Y, Zhou WJ, Zuo WF, Zhan G, and Han B
- Abstract
Developing efficient strategies for synthesizing novel diazocine compounds is valuable because their use has been limited by their synthetic accessibility. This work describes the catalytic (4+3) cycloaddition reaction of carbonyl ylides with azoalkenes generated in situ . The rhodium-catalyzed cascade reaction features good atom and step economy, providing the first access to oxo-bridged diazocines. The product could be synthesized on a gram scale and converted into diversely substituted dihydroisobenzofurans.
- Published
- 2022
- Full Text
- View/download PDF
15. CML/RAGE Signal Bridges a Common Pathogenesis Between Atherosclerosis and Non-alcoholic Fatty Liver.
- Author
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Pang Q, Sun Z, Shao C, Cai H, Bao Z, Wang L, Li L, Jing L, Zhang L, and Wang Z
- Abstract
Non-alcoholic fatty liver disease (NAFLD) has become a common chronic disease in the world. NAFLD is not only a simple intrahepatic lesion, but also affects the occurrence of a variety of extrahepatic complications. In particular, cardiovascular complications are particularly serious, which is the main cause of death in patients with NAFLD. To study the relationship between NAFLD and AS may be a new way to improve the quality of life in patients with NAFLD. As we all known, inflammatory response plays an important role in the occurrence and development of NAFLD and AS. In this study, we found that the accumulation of Nε-carboxymethyllysine (CML) in the liver leads to hepatic steatosis. CML can induce the expression of interleukin (IL-1β), interleukin (IL-6), tumor necrosis factor (TNF-α), C-reactionprotein (CRP) by binding with advanced glycosylation end-product receptor (RAGE) and accelerate the development of AS. After silencing RAGE expression, the expression of pro-inflammatory cytokines was inhibited and liver and aorta pathological changes were relieved. In conclusion, CML/RAGE signal promotes the progression of non-alcoholic fatty liver disease and atherosclerosis. We hope to provide new ideas for the study of liver vascular dialogue in multi organ communication., (Copyright © 2020 Pang, Sun, Shao, Cai, Bao, Wang, Li, Jing, Zhang and Wang.)
- Published
- 2020
- Full Text
- View/download PDF
16. Macrophage galectin-3 enhances intimal translocation of vascular calcification in diabetes mellitus.
- Author
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Sun Z, Li L, Zhang L, Yan J, Shao C, Bao Z, Liu J, Li Y, Zhou M, Hou L, Jing L, Pang Q, Geng Y, Mao X, Gu W, and Wang Z
- Subjects
- Aged, Aged, 80 and over, Animals, Apolipoproteins E genetics, Cells, Cultured, Diabetic Angiopathies pathology, Diabetic Cardiomyopathies genetics, Diabetic Cardiomyopathies pathology, Extracellular Vesicles metabolism, Female, Humans, Male, Mice, Middle Aged, Myocytes, Smooth Muscle metabolism, Tibial Arteries metabolism, Tibial Arteries pathology, Tunica Intima pathology, Vascular Calcification pathology, Diabetic Angiopathies metabolism, Diabetic Cardiomyopathies metabolism, Galectin 3 metabolism, Macrophages metabolism, Tunica Intima metabolism, Vascular Calcification metabolism
- Abstract
The clinical risks and prognosis of diabetic vascular intimal calcification (VIC) and medial calcification (VMC) are different. This study aims to investigate the mechanism of VIC/VMC translocation. Anterior tibial arteries were collected from patients with diabetic foot amputation. The patients were then divided into VIC and VMC groups. There were plaques in all anterior tibial arteries, while the enrichment of galectin-3 in arterial plaques in the VIC group was significantly higher than that in the VMC group. Furthermore, a macrophage/vascular smooth muscle cell (VSMC) coculture system was constructed. VSMC-derived extracellular vesicles (EVs) was labeled with fluorescent probe. After macrophages were pretreated with recombinant galectin-3 protein, the migration of VSMC-derived EVs and VSMC-derived calcification was more pronounced. And anti-galectin-3 antibody can inhibit this process of EVs and calcification translocation. Then, lentivirus (LV)-treated bone marrow cells (BMCs) were transplanted into apolipoprotein E-deficient (ApoE
-/- ) mice, and a diabetic atherosclerosis mouse model was constructed. After 15 wk of high-fat diet, ApoE-/- mice transplanted with LV-shgalectin-3 BMCs exhibited medial calcification and a concentrated distribution of EVs in the media. In conclusion, upregulation of galectin-3 in macrophages promotes the migration of VSMC-derived EVs to the intima and induces diabetic vascular intimal calcification. NEW & NOTEWORTHY The clinical risk and prognosis of vascular intimal and medial calcification are different. Macrophage galectin-3 regulates the migration of vascular smooth muscle cell-derived extracellular vesicles and mediates diabetic vascular intimal/medial calcification translocation. This study may provide insights into the early intervention in diabetic vascular calcification.- Published
- 2020
- Full Text
- View/download PDF
17. N ε -Carboxymethyl-Lysine Negatively Regulates Foam Cell Migration via the Vav1/Rac1 Pathway.
- Author
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Bao Z, Zhang L, Li L, Yan J, Pang Q, Sun Z, Geng Y, Jing L, Shao C, and Wang Z
- Subjects
- Amputation, Surgical, Animals, Apolipoproteins E genetics, Atherosclerosis pathology, Cell Movement, Cells, Cultured, Diabetic Foot pathology, Humans, Lysine metabolism, Mice, Mice, Knockout, Signal Transduction, Apolipoproteins E metabolism, Atherosclerosis metabolism, Diabetic Foot metabolism, Foam Cells physiology, Lysine analogs & derivatives, Proto-Oncogene Proteins c-vav metabolism, rac1 GTP-Binding Protein metabolism
- Abstract
Background: Macrophage-derived foam cells play a central role in atherosclerosis, and their ultimate fate includes apoptosis, promotion of vascular inflammation, or migration to other tissues. N ε -Carboxymethyl-lysine (CML), the key active component of advanced glycation end products, induced foam cell formation and apoptosis. Previous studies have shown that the Vav1/Rac1 pathway affects the macrophage cytoskeleton and cell migration, but its role in the pathogenesis of diabetic atherosclerosis is unknown., Methods and Results: In this study, we used anterior tibiofibular vascular samples from diabetic foot amputation patients and accident amputation patients, and histological and cytological tests were performed using a diabetic ApoE
-/- mouse model and primary peritoneal macrophages, respectively. The results showed that the atherosclerotic plaques of diabetic foot amputation patients and diabetic ApoE-/- mice were larger than those of the control group. Inhibition of the Vav1/Rac1 pathway reduced vascular plaques and promoted the migration of macrophages to lymph nodes. Transwell and wound healing assays showed that the migratory ability of macrophage-derived foam cells was inhibited by CML. Cytoskeletal staining showed that advanced glycation end products inhibited the formation of lamellipodia in foam cells, and inhibition of the Vav1/Rac1 pathway restored the formation of lamellipodia., Conclusion: CML inhibits the migration of foam cells from blood vessels via the Vav1/Rac1 pathway, and this process affects the formation of lamellipodia., Competing Interests: The authors declare that they have no competing interests., (Copyright © 2020 Zhengyang Bao et al.)- Published
- 2020
- Full Text
- View/download PDF
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