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学者姓名：臧伟进
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Abstract ：
Mitochondrial epigenetics is rising as intriguing notion for its potential involvement in aging and diseases, while the details remain largely unexplored. Here it is shown that among the 13 mitochondrial DNA (mtDNA) encoded genes, NADH-dehydrogenase 6 (ND6) transcript is primarily decreased in obese and type 2 diabetes populations, which negatively correlates with its distinctive hypermethylation. Hepatic mtDNA sequencing in mice unveils that ND6 presents the highest methylation level, which dramatically increases under diabetic condition due to enhanced mitochondrial translocation of DNA methyltransferase 1 (DNMT1) promoted by free fatty acid through adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) activation. Hepatic knockdown of ND6 or overexpression of Dnmt1 similarly impairs mitochondrial function and induces systemic insulin resistance both in vivo and in vitro. Genetic or chemical targeting hepatic DNMT1 shows significant benefits against insulin resistance associated metabolic disorders. These findings highlight the pivotal role of ND6 epigenetic network in regulating mitochondrial function and onset of insulin resistance, shedding light on potential preventive and therapeutic strategies of insulin resistance and related metabolic disorders from a perspective of mitochondrial epigenetics.
Keyword ：
dehydrogenase 6 (ND6) DNA methyltransferase 1 (DNMT1) insulin resistance mitochondrial dysfunction mitochondrial NADH‐ obesity and type 2 diabetes mellitus (T2DM)
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| GB/T 7714 | Cao, Ke , Lv, Weiqiang , Wang, Xueqiang et al. Hypermethylation of Hepatic Mitochondrial ND6 Provokes Systemic Insulin Resistance [J]. | ADVANCED SCIENCE , 2021 , 8 (11) . |
| MLA | Cao, Ke et al. "Hypermethylation of Hepatic Mitochondrial ND6 Provokes Systemic Insulin Resistance" . | ADVANCED SCIENCE 8 . 11 (2021) . |
| APA | Cao, Ke , Lv, Weiqiang , Wang, Xueqiang , Dong, Shanshan , Liu, Xuyun , Yang, Tielin et al. Hypermethylation of Hepatic Mitochondrial ND6 Provokes Systemic Insulin Resistance . | ADVANCED SCIENCE , 2021 , 8 (11) . |
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Abstract ：
Mitochondria participate in essential cellular functions, including energy production, metabolism, redox homeostasis regulation, intracellular Ca2+ handling, apoptosis, and cell fate determination. Disruption of mitochondrial homeostasis under pathological conditions results in mitochondrial reactive oxygen species (ROS) generation and energy insufficiency, which further disturb mitochondrial and cellular homeostasis in a deleterious loop. Mitochondrial redox status has therefore become a potential target for therapy against cardiovascular diseases. In this review, we highlight recent progress in determining the roles of mitochondrial processes in regulating mitochondrial redox status, including mitochondrial dynamics (fusion-fission pathways), mitochondrial cristae remodeling, mitophagy, biogenesis, and mitochondrion-organelle interactions (endoplasmic reticulum-mitochondrion interactions, nucleus-mitochondrion communication, and lipid droplet-mitochondrion interactions). The strategies that activate vagal system include direct vagal activation (electrical vagal stimulation and administration of vagal neurotransmitter acetylcholine) and pharmacological modulation (choline and cholinesterase inhibitors). The vagal system plays an important role in maintaining mitochondrial homeostasis and suppressing mitochondrial oxidative stress by promoting mitochondrial biogenesis and mitophagy, moderating mitochondrial fusion and fission, strengthening mitochondrial cristae stabilization, regulating mitochondrion-organelle interactions, and inhibiting mitochondrial Ca2+ overload. Therefore, enhancement of vagal activity can maintain mitochondrial homeostasis and represents a promising therapeutic strategy for cardiovascular diseases.
Keyword ：
Cardiovascular diseases Mitochondrial homeostasis Mitochondrial redox status Mitochondrion–organelle interactions Vagal activity
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| GB/T 7714 | He Xi , Liu Jiankang , Zang Wei-Jin . Mitochondrial homeostasis and redox status in cardiovascular diseases: Protective role of the vagal system. [J]. | Free radical biology & medicine , 2021 , 178 : 369-379 . |
| MLA | He Xi et al. "Mitochondrial homeostasis and redox status in cardiovascular diseases: Protective role of the vagal system." . | Free radical biology & medicine 178 (2021) : 369-379 . |
| APA | He Xi , Liu Jiankang , Zang Wei-Jin . Mitochondrial homeostasis and redox status in cardiovascular diseases: Protective role of the vagal system. . | Free radical biology & medicine , 2021 , 178 , 369-379 . |
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Abstract ：
Choline attenuates abdominal aortic coarctation-induced cardiac remodeling and cardiac dysfunction, by amelioration of circadian rhythm disruption and attenuation of calcium-handling protein defects. Modulation of vagal activity by choline may have therapeutic potential for cardiac remodeling and heart failure. The key pathophysiological process leading to heart failure is cardiac remodeling, a term referring to cardiac hypertrophy, fibrosis, and apoptosis. We explored circadian rhythm disruption and calcium dyshomeostasis in cardiac remodeling and investigated the cardioprotective effect of choline. The experiments were conducted using a model of cardiac remodeling by abdominal aorta coarctation (AAC) in Sprague-Dawley rats. In vitro cardiomyocyte remodeling was induced by exposing neonatal rat cardiomyocytes to angiotensin II. The circadian rhythms of the transcript levels of the seven major components of the mammalian clock (Bmal1, Clock, Rev-erb alpha, Per1/2, and Cry1/2) were altered in AAC rat hearts during a normal 24 h light/dark cycle. AAC also upregulated the levels of proteins that mediate store-operated Ca2+ entry/receptor-operated Ca2+ entry (stromal interaction molecule 1 [STIM1], Orai1, and transient receptor potential canonical 6 [TRPC6]) in rat hearts. Moreover, choline ameliorated circadian rhythm disruption, reduced the upregulated protein levels of STIM1, Orai1, and TRPC6, and alleviated cardiac dysfunction and remodeling (evidenced by attenuated cardiac hypertrophy, fibrosis, and apoptosis) in AAC rats. In vitro analyses showed that choline ameliorated calcium overload, downregulated STIM1, Orai1, and TRPC6, and inhibited thapsigargin-induced store-operated Ca2+ entry and 1-oleoyl-2-acetyl-sn-glycerol-induced receptor-operated Ca2+ entry in angiotensin II-treated cardiomyocytes. In conclusion, choline attenuated AAC-induced cardiac remodeling and cardiac dysfunction, which was related to amelioration of circadian rhythm disruption and attenuation of calcium-handling protein defects. Modulation of vagal activity by choline targeting the circadian rhythm and calcium homeostasis may have therapeutic potential for cardiac remodeling and heart failure.
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| GB/T 7714 | He, Xi , Yang, Si , Deng, Juan et al. Amelioration of circadian disruption and calcium-handling protein defects by choline alleviates cardiac remodeling in abdominal aorta coarctation rats [J]. | LABORATORY INVESTIGATION , 2021 , 101 (7) : 878-896 . |
| MLA | He, Xi et al. "Amelioration of circadian disruption and calcium-handling protein defects by choline alleviates cardiac remodeling in abdominal aorta coarctation rats" . | LABORATORY INVESTIGATION 101 . 7 (2021) : 878-896 . |
| APA | He, Xi , Yang, Si , Deng, Juan , Wu, Qing , Zang, Wei-Jin . Amelioration of circadian disruption and calcium-handling protein defects by choline alleviates cardiac remodeling in abdominal aorta coarctation rats . | LABORATORY INVESTIGATION , 2021 , 101 (7) , 878-896 . |
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Abstract ：
As a key organelle in eukaryotic cells, mitochondria play a central role in maintaining normal cellular functions. Mitochondrial dysfunction is reported to be closely related with aging and various diseases. Epigenetic modifications in nuclear genome provide a substantial layer for the modulation of nuclear-encoded gene expression. However, whether mitochondria could also be subjected to such similar epigenetic alterations and the involved mechanisms remain largely obscure and controversial. Recently, accumulating evidence has suggested that mitochondrial epigenetics, also known as mitoepigenetics may serve as an intriguing regulatory layer in mitochondrial DNA (mtDNA)-encoded gene expression. Given the potential regulatory role of mitoepigenetics, mitochondrial dysfunction derived from mitoepigenetics-induced abnormal gene expression could also be closely associated with aging and disease development. In this review, we summarized the recent advances in mitoepigenetics, with a special focus on mtDNA methylation in aging and metabolic-related diseases as well as the new methods and technologies for the study of mitoepigenetics. Uncovering the regulatory role of mitoepigenetics will help to understand the underlying mechanisms of mitochondrial dysfunction and provide novel strategies for delaying aging and preventing metabolic-related diseases.
Keyword ：
Mitochondrial DNA (mtDNA) methylation Mitochondrial epigenetics (mitoepigenetics) Mitochondrial non-coding RNAs (ncRNAs) mtDNA-associated proteins Post-translational modifications (PTMs)
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| GB/T 7714 | Cao, Ke , Feng, Zhihui , Gao, Feng et al. Mitoepigenetics: An intriguing regulatory layer in aging and metabolic-related diseases [J]. | FREE RADICAL BIOLOGY AND MEDICINE , 2021 , 177 : 337-346 . |
| MLA | Cao, Ke et al. "Mitoepigenetics: An intriguing regulatory layer in aging and metabolic-related diseases" . | FREE RADICAL BIOLOGY AND MEDICINE 177 (2021) : 337-346 . |
| APA | Cao, Ke , Feng, Zhihui , Gao, Feng , Zang, Weijin , Liu, Jiankang . Mitoepigenetics: An intriguing regulatory layer in aging and metabolic-related diseases . | FREE RADICAL BIOLOGY AND MEDICINE , 2021 , 177 , 337-346 . |
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Abstract ：
The disruption of gut microbes is associated with diabetic cardiomyopathy, but the mechanism by which gut microbes affect cardiac damage remains unclear. We explored gut microbes and branched-chain amino acid (BCAA) metabolite catabolism in diabetic cardiomyopathy mice and investigated the cardioprotective effect of pyridostigmine. The experiments were conducted using a model of diabetic cardiomyopathy induced by a high-fat diet + streptozotocin in C57BL/6 mice. The results of high-throughput sequencing showed that diabetic cardiomyopathy mice exhibited decreased gut microbial diversity, altered abundance of the diabetes-related microbes, and increased abundance of the BCAA-producing microbes Clostridiales and Lachnospiraceae. In addition, diabetes downregulated tight junction proteins (ZO-1, occludin, and claudin-1) and increased intestinal permeability to impair the intestinal barrier. These impairments were accompanied by reduction in vagal activity that manifested as increased acetylcholinesterase levels, decreased acetylcholine levels, and heart rate variability, which eventually led to cardiac damage. Pyridostigmine enhanced vagal activity, restored gut microbiota homeostasis, decreased BCAA-producing microbe abundance, and improved the intestinal barrier to reduce circulating BCAA levels. Pyridostigmine also upregulated BCAT2 and PP2Cm and downregulated p-BCKDHA/BCKDHA and BCKDK to improve cardiac BCAA catabolism. Moreover, pyridostigmine alleviated abnormal mitochondrial structure; increased ATP production; decreased reactive oxygen species and mitochondria-related apoptosis; and attenuated cardiac dysfunction, hypertrophy, and fibrosis in diabetic cardiomyopathy mice. In conclusion, the gut microbiota, BCAA catabolism, and vagal activity were impaired in diabetic cardiomyopathy mice but were improved by pyridostigmine. These results provide novel insights for the development of a therapeutic strategy for diabetes-induced cardiac damage that targets gut microbes and BCAA catabolism.
Keyword ：
branched-chain amino acids diabetic cardiomyopathy gut microbiota mitochondrial dysfunction pyridostigmine vagal activity
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| GB/T 7714 | Yang, Yang , Zhao, Ming , He, Xi et al. Pyridostigmine Protects Against Diabetic Cardiomyopathy by Regulating Vagal Activity, Gut Microbiota, and Branched-Chain Amino Acid Catabolism in Diabetic Mice [J]. | FRONTIERS IN PHARMACOLOGY , 2021 , 12 . |
| MLA | Yang, Yang et al. "Pyridostigmine Protects Against Diabetic Cardiomyopathy by Regulating Vagal Activity, Gut Microbiota, and Branched-Chain Amino Acid Catabolism in Diabetic Mice" . | FRONTIERS IN PHARMACOLOGY 12 (2021) . |
| APA | Yang, Yang , Zhao, Ming , He, Xi , Wu, Qing , Li, Dong-Ling , Zang, Wei-Jin . Pyridostigmine Protects Against Diabetic Cardiomyopathy by Regulating Vagal Activity, Gut Microbiota, and Branched-Chain Amino Acid Catabolism in Diabetic Mice . | FRONTIERS IN PHARMACOLOGY , 2021 , 12 . |
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Abstract ：
Lipid droplets (LDs), which are neutral lipid storage organelles, are important for lipid metabolism and energy homeostasis. LD lipolysis and interactions with mitochondria are tightly coupled to cellular metabolism and may be potential targets to buffer the effects of excessive toxic lipid species levels. Acetylcholine (ACh), the major neurotransmitter of the vagus nerve, exhibits cardioprotective effects. However, limited research has focused on its effects on LD lipolysis and the LD-mitochondria association in fatty acid (FA) overload models. Here, we reveal that palmitate (PA) induces an increase in expression of the FA transport protein cluster of differentiation 36 (CD36) and LD formation; remarkably reduces the expression of lipases involved in triacylglycerol (TAG) lipolysis, such as adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL) and monoacylglycerol lipase (MGL); impairs LD-mitochondria interaction; and decreases perilipin 5 (PLIN5) expression, resulting in LD accumulation and mitochondrial dysfunction, which ultimately lead to cardiomyocyte apoptosis. ACh significantly upregulates PLIN5 expression and improved LD lipolysis and the LD-mitochondria association. Moreover, ACh reduces CD36 expression, LD deposition and mitochondrial dysfunction, ultimately suppressing apoptosis in PA-treated neonatal rat ventricular cardiomyocytes (NRVCs). Knockdown of PLIN5, which plays a role in LD-mitochondria contact site formation, abolishes the protective effects of ACh in PA-treated NRVCs. Thus, ACh protects cardiomyocytes from PA-induced apoptosis, at least partly, by promoting LD lipolysis and activating LD-mitochondria interactions via PLIN5. These findings may aid in developing novel therapeutic approaches that target LD lipolysis and PLIN5-mediated LD-mitochondria interactions to prevent or alleviate lipotoxic cardiomyopathy.
Keyword ：
acetylcholine cardiomyocyte apoptosis lipid droplet lipolysis lipid droplet-mitochondria interaction palmitate perilipin 5
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| GB/T 7714 | Wu, Qing , Zhao, Ming , He, Xi et al. Acetylcholine reduces palmitate-induced cardiomyocyte apoptosis by promoting lipid droplet lipolysis and perilipin 5-mediated lipid droplet-mitochondria interaction [J]. | CELL CYCLE , 2021 , 20 (18) : 1890-1906 . |
| MLA | Wu, Qing et al. "Acetylcholine reduces palmitate-induced cardiomyocyte apoptosis by promoting lipid droplet lipolysis and perilipin 5-mediated lipid droplet-mitochondria interaction" . | CELL CYCLE 20 . 18 (2021) : 1890-1906 . |
| APA | Wu, Qing , Zhao, Ming , He, Xi , Xue, Runqing , Li, Dongling , Yu, Xiaojiang et al. Acetylcholine reduces palmitate-induced cardiomyocyte apoptosis by promoting lipid droplet lipolysis and perilipin 5-mediated lipid droplet-mitochondria interaction . | CELL CYCLE , 2021 , 20 (18) , 1890-1906 . |
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Abstract ：
White adipose tissue (WAT) expansion in obesity occurs through enlargement of preexisting adipocytes (hypertrophy) and through formation of new adipocytes (adipogenesis). Adipogenesis results in WAT hyperplasia, smaller adipocytes and a metabolically more favourable form of obesity. How obesogenic WAT hyperplasia is induced remains, however, poorly understood. Here, we show that the mechanosensitive cationic channel Piezo1 mediates diet-induced adipogenesis. Mice lacking Piezo1 in mature adipocytes demonstrated defective differentiation of preadipocyte into mature adipocytes when fed a high fat diet (HFD) resulting in larger adipocytes, increased WAT inflammation and reduced insulin sensitivity. Opening of Piezo1 in mature adipocytes causes the release of the adipogenic fibroblast growth factor 1 (FGF1), which induces adipocyte precursor differentiation through activation of the FGF-receptor-1. These data identify a central feed-back mechanism by which mature adipocytes control adipogenesis during the development of obesity and suggest Piezo1-mediated adipocyte mechano-signalling as a mechanism to modulate obesity and its metabolic consequences. Adipose tissue expansion occurs via enlargement of adipocytes as well as the generation of new fat cells, the latter being associated with more favorable metabolic outcomes. Here, the authors show that activation of adipocyte Piezo1 results in release of FGF1 and stimulates the differentiation of adipocyte precursor cells.
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| GB/T 7714 | Wang, ShengPeng , Cao, Shuang , Arhatte, Malika et al. Adipocyte Piezo1 mediates obesogenic adipogenesis through the FGF1/FGFR1 signaling pathway in mice [J]. | NATURE COMMUNICATIONS , 2020 , 11 (1) . |
| MLA | Wang, ShengPeng et al. "Adipocyte Piezo1 mediates obesogenic adipogenesis through the FGF1/FGFR1 signaling pathway in mice" . | NATURE COMMUNICATIONS 11 . 1 (2020) . |
| APA | Wang, ShengPeng , Cao, Shuang , Arhatte, Malika , Li, Dahui , Shi, Yue , Kurz, Sabrina et al. Adipocyte Piezo1 mediates obesogenic adipogenesis through the FGF1/FGFR1 signaling pathway in mice . | NATURE COMMUNICATIONS , 2020 , 11 (1) . |
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Abstract ：
Hyperlipidemia is associated with metabolic disorders, but the detailed mechanisms and related interventions remain largely unclear. As a functional food in Asian diets, Herba houttuyniae has been reported to have beneficial effects on health. The present research was to investigate the protective effects of Herba houttuyniae aqueous extract (HAE) on hyperlipidemia-induced liver and heart impairments and its potential mechanisms. Male C57BL/6J mice were administered with 200 or 400 mg/kg/day HAE for 9 days, followed by intraperitoneal injection with 0.5 g/kg poloxamer 407 to induce acute hyperlipidemia. HAE treatment significantly attenuated excessive serum lipids and tissue damage markers, prevented hepatic lipid deposition, improved cardiac remodeling, and ameliorated hepatic and cardiac oxidative stress induced by hyperlipidemia. More importantly, NF-E2 related factor (Nrf2)-mediated antioxidant and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha)-mediated mitochondrial biogenesis pathways as well as mitochondrial complex activities were downregulated in the hyperlipidemic mouse livers and hearts, which may be attributable to the loss of adenosine monophosphate (AMP)-activated protein kinase (AMPK) activity: all of these changes were reversed by HAE supplementation. Our findings link the AMPK/PGC-1 alpha/Nrf2 cascade to hyperlipidemia-induced liver and heart impairments and demonstrate the protective effect of HAE as an AMPK activator in the prevention of hyperlipidemia-related diseases.
Keyword ：
AMP-activated protein kinase Herba houttuyniae hyperlipidemia mitochondrial biogenesis oxidative stress
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| GB/T 7714 | Cao, Ke , Lv, Weiqiang , Liu, Xuyun et al. Herba houttuyniae Extract Benefits Hyperlipidemic Mice via Activation of the AMPK/PGC-1 alpha/Nrf2 Cascade [J]. | NUTRIENTS , 2020 , 12 (1) . |
| MLA | Cao, Ke et al. "Herba houttuyniae Extract Benefits Hyperlipidemic Mice via Activation of the AMPK/PGC-1 alpha/Nrf2 Cascade" . | NUTRIENTS 12 . 1 (2020) . |
| APA | Cao, Ke , Lv, Weiqiang , Liu, Xuyun , Fan, Yingying , Wang, Kexin , Feng, Zhihui et al. Herba houttuyniae Extract Benefits Hyperlipidemic Mice via Activation of the AMPK/PGC-1 alpha/Nrf2 Cascade . | NUTRIENTS , 2020 , 12 (1) . |
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Abstract ：
Objective: Cyclooxygenase (COX)-2, an inducible isoform of the major rate-limiting enzymes that regulate the production of prostaglandins is associated with injury, inflammation and proliferation. We sought to examine whether plasma COX-2 levels and its genetic variants is associated with salt sensitivity, BP changes and/or hypertension in humans. Methods: Eighty participants (aged 18-65 years) were maintained sequentially either on a usual diet for 3 days, a low-salt diet (3.0 g) for 7 days, and a high-salt diet (18.0 g) for an additional 7 days. In addition, we studied participants of the original Baoji Salt-Sensitive Study, recruited from 124 families from seven Chinese villages in 2004 who received the same salt intake intervention, and evaluated them for the development of hypertension. Results: Plasma COX-2 levels were significantly decreased with reduction of salt intake from the usual to a low-salt diet and decreased further when converting from the low-salt to the high-salt diet. SNPs rs12042763 in theCOX-2gene was significantly associated with SBP responses to both low-salt and high-salt diet. SNPs rs689466 and rs12042763 were significantly associated with longitudinal changes in BPs. In addition, several COX-2 SNPs were significantly associated with incident hypertension over an 8-year follow-up. Gene-based analyses also supported the overall association of COX-2 with longitudinal changes in SBP and hypertension incidence. Conclusion: This study shows that dietary salt intake affects plasma COX-2 levels and that COX-2 may play a role in salt sensitivity, BP progression and development of hypertension in the Chinese populations studied.
Keyword ：
blood pressure COX-2 gene polymorphism salt salt sensitivity
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| GB/T 7714 | Wang, Yang , Zhou, Qing , Gao, Wei-Hua et al. Association of plasma cyclooxygenase-2 levels and genetic polymorphisms with salt sensitivity, blood pressure changes and hypertension incidence in Chinese adults [J]. | JOURNAL OF HYPERTENSION , 2020 , 38 (9) : 1745-1754 . |
| MLA | Wang, Yang et al. "Association of plasma cyclooxygenase-2 levels and genetic polymorphisms with salt sensitivity, blood pressure changes and hypertension incidence in Chinese adults" . | JOURNAL OF HYPERTENSION 38 . 9 (2020) : 1745-1754 . |
| APA | Wang, Yang , Zhou, Qing , Gao, Wei-Hua , Yan, Yu , Chu, Chao , Chen, Chen et al. Association of plasma cyclooxygenase-2 levels and genetic polymorphisms with salt sensitivity, blood pressure changes and hypertension incidence in Chinese adults . | JOURNAL OF HYPERTENSION , 2020 , 38 (9) , 1745-1754 . |
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Abstract ：
Phenotypic switching of vascular smooth muscle cells (VSMCs) plays a critical role in atherosclerosis, vascular restenosis, and hypertension. Choline exerts cardioprotective effects; however, little is known about its effects on VSMC phenotypic switching and vascular remodeling. Here, we investigated whether choline modulates VSMC phenotypic changes and explored the underlying mechanisms. Approach and Results: In cultured VSMCs, choline promoted Nrf2 (nuclear factor erythroid 2-related factor 2) nuclear translocation, inducing the expression of HO-1 (heme oxygenase-1) and NQO-1 (NAD[P]H quinone oxidoreductase-1). Consequently, choline ameliorated Ang II (angiotensin II)-induced increases in NOX (NAD[P]H oxidase) expression and the mitochondrial reactive oxygen species level, thereby attenuating Ang II-induced VSMC phenotypic switching, proliferation, and migration, presumably via M3AChRs (type 3 muscarinic acetylcholine receptors). Downregulation of M3AChR or Nrf2 diminished choline-mediated upregulation of Nrf2, HO-1, and NQO-1 expression, as well as inhibition of VSMC phenotypic transformation, suggesting that M3AChR and Nrf2 activation are responsible for the protective effects of choline. Moreover, activation of the Nrf2 pathway by sulforaphane suppressed Ang II-induced VSMC phenotypic switching and proliferation, indicating that Nrf2 is a key regulator of VSMC phenotypic switching and vascular homeostasis. In a rat model of abdominal aortic constriction in vivo, choline attenuated VSMC phenotypic transformation and vascular remodeling in a manner related to activation of the Nrf2 pathway.These results reveal that choline impedes VSMC phenotypic switching, proliferation, migration, and vascular remodeling by activating M3AChR and Nrf2-antioxidant signaling and suggest a novel role for Nrf2 in VSMC phenotypic modulation.
Keyword ：
angiotensin II muscarinic agonists myocytes, smooth muscle oxidative stress vascular remodeling
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| GB/T 7714 | He Xi , Deng Juan , Yu Xiao-Jiang et al. Activation of M3AChR (Type 3 Muscarinic Acetylcholine Receptor) and Nrf2 (Nuclear Factor Erythroid 2-Related Factor 2) Signaling by Choline Alleviates Vascular Smooth Muscle Cell Phenotypic Switching and Vascular Remodeling. [J]. | Arteriosclerosis, thrombosis, and vascular biology , 2020 , 40 (11) : 2649-2664 . |
| MLA | He Xi et al. "Activation of M3AChR (Type 3 Muscarinic Acetylcholine Receptor) and Nrf2 (Nuclear Factor Erythroid 2-Related Factor 2) Signaling by Choline Alleviates Vascular Smooth Muscle Cell Phenotypic Switching and Vascular Remodeling." . | Arteriosclerosis, thrombosis, and vascular biology 40 . 11 (2020) : 2649-2664 . |
| APA | He Xi , Deng Juan , Yu Xiao-Jiang , Yang Si , Yang Yang , Zang Wei-Jin . Activation of M3AChR (Type 3 Muscarinic Acetylcholine Receptor) and Nrf2 (Nuclear Factor Erythroid 2-Related Factor 2) Signaling by Choline Alleviates Vascular Smooth Muscle Cell Phenotypic Switching and Vascular Remodeling. . | Arteriosclerosis, thrombosis, and vascular biology , 2020 , 40 (11) , 2649-2664 . |
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