{"title":"盐促进炎症:机制学见解","authors":"E. Ros","doi":"10.20455/ros.2022.n.801","DOIUrl":null,"url":null,"abstract":"It has been well established that high dietary salt intake promotes inflammation and contributes to the pathogenesis of many inflammatory disorders, especially cardiovascular diseases. Several recent studies published in prestigious journals have further elucidated the molecular pathways underlying high salt-induced inflammation, including identification of the involvement of mitochondrial electron transport chain and the Nrf2-SIRT3 signaling axis. These novel findings provide important mechanistic insights and offer potential opportunities for developing modalities for intervention of high salt-associated pathophysiological conditions.\n(First online: March 1, 2022)\nREFERENCES\n\nThornton SN. Sodium intake, cardiovascular disease, and physiology. Nat Rev Cardiol 2018; 15(8):497. doi: https://dx.doi.org/10.1038/s41569-018-0047-3\nCook NR, He FJ, MacGregor GA, Graudal N. Sodium and health-concordance and controversy. BMJ 2020; 369:m2440. doi: https://dx.doi.org/10.1136/bmj.m2440\nWu C, Yosef N, Thalhamer T, Zhu C, Xiao S, Kishi Y, et al. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature 2013; 496(7446):513–7. doi: https://dx.doi.org/10.1038/nature11984\nWilck N, Matus MG, Kearney SM, Olesen SW, Forslund K, Bartolomaeus H, et al. Salt-responsive gut commensal modulates TH17 axis and disease. Nature 2017; 551(7682):585–9. doi: https://dx.doi.org/10.1038/nature24628\nZhang WC, Zheng XJ, Du LJ, Sun JY, Shen ZX, Shi C, et al. High salt primes a specific activation state of macrophages, M(Na). Cell Res 2015; 25(8):893–910. doi: https://dx.doi.org/10.1038/cr.2015.87\nGeisberger S, Bartolomaeus H, Neubert P, Willebrand R, Zasada C, Bartolomaeus T, et al. Salt Transiently inhibits mitochondrial energetics in mononuclear phagocytes. Circulation 2021; 144(2):144–58. doi: https://dx.doi.org/10.1161/CIRCULATIONAHA.120.052788\nRos EO. Sodium ion regulates mitochondrial ROS. React Oxyg Species (Apex) 2021; 11:n5–n6. doi: https://dx.doi.org/10.20455/ros.2021.n.805.\nShadel GS, Horvath TL. Mitochondrial ROS signaling in organismal homeostasis. Cell 2015; 163(3):560–9. doi: https://dx.doi.org/10.1016/j.cell.2015.10.001\nLanaspa MA, Kuwabara M, Andres-Hernando A, Li N, Cicerchi C, Jensen T, et al. High salt intake causes leptin resistance and obesity in mice by stimulating endogenous fructose production and metabolism. Proc Natl Acad Sci USA 2018; 115(12):3138–43. doi: https://dx.doi.org/10.1073/pnas.1713837115\nGao P, You M, Li L, Zhang Q, Fang X, Wei X, et al. Salt-Induced hepatic inflammatory memory contributes to cardiovascular damage through epigenetic modulation of SIRT3. Circulation 2022; 145(5):375–91. doi: https://dx.doi.org/10.1161/CIRCULATIONAHA.121.055600\nDikalova AE, Pandey A, Xiao L, Arslanbaeva L, Sidorova T, Lopez MG, et al. Mitochondrial deacetylase Sirt3 reduces vascular dysfunction and hypertension while Sirt3 depletion in essential hypertension is linked to vascular inflammation and oxidative stress. Circ Res 2020; 126(4):439–52. doi: https://dx.doi.org/10.1161/CIRCRESAHA.119.315767\nKim A, Koo JH, Lee JM, Joo MS, Kim TH, Kim H, et al. NRF2-mediated SIRT3 induction protects hepatocytes from ER stress-induced liver injury. FASEB J 2022; 36(3):e22170. doi: https://dx.doi.org/10.1096/fj.202101470R\n","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2022-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Salt Promotes Inflammation: Mechanistic Insights\",\"authors\":\"E. Ros\",\"doi\":\"10.20455/ros.2022.n.801\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"It has been well established that high dietary salt intake promotes inflammation and contributes to the pathogenesis of many inflammatory disorders, especially cardiovascular diseases. Several recent studies published in prestigious journals have further elucidated the molecular pathways underlying high salt-induced inflammation, including identification of the involvement of mitochondrial electron transport chain and the Nrf2-SIRT3 signaling axis. These novel findings provide important mechanistic insights and offer potential opportunities for developing modalities for intervention of high salt-associated pathophysiological conditions.\\n(First online: March 1, 2022)\\nREFERENCES\\n\\nThornton SN. Sodium intake, cardiovascular disease, and physiology. Nat Rev Cardiol 2018; 15(8):497. doi: https://dx.doi.org/10.1038/s41569-018-0047-3\\nCook NR, He FJ, MacGregor GA, Graudal N. Sodium and health-concordance and controversy. BMJ 2020; 369:m2440. doi: https://dx.doi.org/10.1136/bmj.m2440\\nWu C, Yosef N, Thalhamer T, Zhu C, Xiao S, Kishi Y, et al. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature 2013; 496(7446):513–7. doi: https://dx.doi.org/10.1038/nature11984\\nWilck N, Matus MG, Kearney SM, Olesen SW, Forslund K, Bartolomaeus H, et al. Salt-responsive gut commensal modulates TH17 axis and disease. Nature 2017; 551(7682):585–9. doi: https://dx.doi.org/10.1038/nature24628\\nZhang WC, Zheng XJ, Du LJ, Sun JY, Shen ZX, Shi C, et al. High salt primes a specific activation state of macrophages, M(Na). Cell Res 2015; 25(8):893–910. doi: https://dx.doi.org/10.1038/cr.2015.87\\nGeisberger S, Bartolomaeus H, Neubert P, Willebrand R, Zasada C, Bartolomaeus T, et al. Salt Transiently inhibits mitochondrial energetics in mononuclear phagocytes. Circulation 2021; 144(2):144–58. doi: https://dx.doi.org/10.1161/CIRCULATIONAHA.120.052788\\nRos EO. Sodium ion regulates mitochondrial ROS. React Oxyg Species (Apex) 2021; 11:n5–n6. doi: https://dx.doi.org/10.20455/ros.2021.n.805.\\nShadel GS, Horvath TL. Mitochondrial ROS signaling in organismal homeostasis. Cell 2015; 163(3):560–9. doi: https://dx.doi.org/10.1016/j.cell.2015.10.001\\nLanaspa MA, Kuwabara M, Andres-Hernando A, Li N, Cicerchi C, Jensen T, et al. High salt intake causes leptin resistance and obesity in mice by stimulating endogenous fructose production and metabolism. Proc Natl Acad Sci USA 2018; 115(12):3138–43. doi: https://dx.doi.org/10.1073/pnas.1713837115\\nGao P, You M, Li L, Zhang Q, Fang X, Wei X, et al. Salt-Induced hepatic inflammatory memory contributes to cardiovascular damage through epigenetic modulation of SIRT3. Circulation 2022; 145(5):375–91. doi: https://dx.doi.org/10.1161/CIRCULATIONAHA.121.055600\\nDikalova AE, Pandey A, Xiao L, Arslanbaeva L, Sidorova T, Lopez MG, et al. Mitochondrial deacetylase Sirt3 reduces vascular dysfunction and hypertension while Sirt3 depletion in essential hypertension is linked to vascular inflammation and oxidative stress. Circ Res 2020; 126(4):439–52. doi: https://dx.doi.org/10.1161/CIRCRESAHA.119.315767\\nKim A, Koo JH, Lee JM, Joo MS, Kim TH, Kim H, et al. NRF2-mediated SIRT3 induction protects hepatocytes from ER stress-induced liver injury. 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引用次数: 0
摘要
高盐饮食摄入促进炎症,并有助于许多炎症性疾病的发病机制,特别是心血管疾病。最近发表在著名期刊上的几项研究进一步阐明了高盐诱导炎症的分子途径,包括线粒体电子传递链和Nrf2-SIRT3信号轴的参与。这些新发现提供了重要的机制见解,并为开发干预高盐相关病理生理状况的模式提供了潜在的机会。(首次在线:2022年3月1日)钠摄入量、心血管疾病和生理。Nat Rev Cardiol 2018;15(8): 497。doi: https://dx.doi.org/10.1038/s41569-018-0047-3Cook NR,何方军,MacGregor GA, Graudal N.钠与健康的一致性和争议。BMJ 2020;369: m2440。doi: https://dx.doi.org/10.1136/bmj.m2440Wu C, Yosef N, Thalhamer T,朱翀,肖松,Kishi Y,等。诱导型盐感激酶SGK1诱导致病性TH17细胞。自然2013;496(7446): 513 - 7。doi: https://dx.doi.org/10.1038/nature11984Wilck N, Matus MG, Kearney SM, Olesen SW, Forslund K, Bartolomaeus H,等。盐反应性肠道共生调节TH17轴和疾病。自然2017;551(7682): 585 - 9。doi: https://dx.doi.org/10.1038/nature24628Zhang王文成,郑晓军,杜立军,孙建勇,沈志祥,石超,等。高盐启动巨噬细胞的特定激活状态,M(Na)。Cell Res 2015;25(8): 893 - 910。doi: https://dx.doi.org/10.1038/cr.2015.87Geisberger S, Bartolomaeus H, Neubert P, Willebrand R, Zasada C, Bartolomaeus T,等。盐暂时抑制单核吞噬细胞的线粒体能量。发行量2021;144(2): 144 - 58。doi: https://dx.doi.org/10.1161/CIRCULATIONAHA.120.052788Ros EO。钠离子调控线粒体活性氧。React Oxyg Species (Apex) 2021;11: n5-n6。doi: https://dx.doi.org/10.20455/ros.2021.n.805.Shadel GS, Horvath TL.线粒体ROS信号在机体内稳态。细胞2015;163(3): 560 - 9。doi: https://dx.doi.org/10.1016/j.cell.2015.10.001Lanaspa MA, Kuwabara M, Andres-Hernando A, Li N, Cicerchi C, Jensen T,等。高盐摄入通过刺激内源性果糖的产生和代谢导致小鼠瘦素抵抗和肥胖。美国国家科学促进会2018;115(12): 3138 - 43。doi: https://dx.doi.org/10.1073/pnas.1713837115Gao P,尤明,李磊,张强,方鑫,魏鑫,等。盐诱导的肝脏炎症记忆通过表观遗传调节SIRT3参与心血管损伤。发行量2022;145(5): 375 - 91。doi: https://dx.doi.org/10.1161/CIRCULATIONAHA.121.055600Dikalova AE, Pandey A, Xiao L, Arslanbaeva L, Sidorova T, Lopez MG等。线粒体去乙酰化酶Sirt3减少血管功能障碍和高血压,而原发性高血压中Sirt3的消耗与血管炎症和氧化应激有关。Circ Res 2020;126(4): 439 - 52。doi: https://dx.doi.org/10.1161/CIRCRESAHA.119.315767Kim A, Koo JH, Lee JM, Joo MS, Kim TH, Kim H,等。nrf2介导的SIRT3诱导可保护肝细胞免受内质网应激性肝损伤。fasb j 2022;36 (3): e22170。doi: https://dx.doi.org/10.1096/fj.202101470R
It has been well established that high dietary salt intake promotes inflammation and contributes to the pathogenesis of many inflammatory disorders, especially cardiovascular diseases. Several recent studies published in prestigious journals have further elucidated the molecular pathways underlying high salt-induced inflammation, including identification of the involvement of mitochondrial electron transport chain and the Nrf2-SIRT3 signaling axis. These novel findings provide important mechanistic insights and offer potential opportunities for developing modalities for intervention of high salt-associated pathophysiological conditions.
(First online: March 1, 2022)
REFERENCES
Thornton SN. Sodium intake, cardiovascular disease, and physiology. Nat Rev Cardiol 2018; 15(8):497. doi: https://dx.doi.org/10.1038/s41569-018-0047-3
Cook NR, He FJ, MacGregor GA, Graudal N. Sodium and health-concordance and controversy. BMJ 2020; 369:m2440. doi: https://dx.doi.org/10.1136/bmj.m2440
Wu C, Yosef N, Thalhamer T, Zhu C, Xiao S, Kishi Y, et al. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature 2013; 496(7446):513–7. doi: https://dx.doi.org/10.1038/nature11984
Wilck N, Matus MG, Kearney SM, Olesen SW, Forslund K, Bartolomaeus H, et al. Salt-responsive gut commensal modulates TH17 axis and disease. Nature 2017; 551(7682):585–9. doi: https://dx.doi.org/10.1038/nature24628
Zhang WC, Zheng XJ, Du LJ, Sun JY, Shen ZX, Shi C, et al. High salt primes a specific activation state of macrophages, M(Na). Cell Res 2015; 25(8):893–910. doi: https://dx.doi.org/10.1038/cr.2015.87
Geisberger S, Bartolomaeus H, Neubert P, Willebrand R, Zasada C, Bartolomaeus T, et al. Salt Transiently inhibits mitochondrial energetics in mononuclear phagocytes. Circulation 2021; 144(2):144–58. doi: https://dx.doi.org/10.1161/CIRCULATIONAHA.120.052788
Ros EO. Sodium ion regulates mitochondrial ROS. React Oxyg Species (Apex) 2021; 11:n5–n6. doi: https://dx.doi.org/10.20455/ros.2021.n.805.
Shadel GS, Horvath TL. Mitochondrial ROS signaling in organismal homeostasis. Cell 2015; 163(3):560–9. doi: https://dx.doi.org/10.1016/j.cell.2015.10.001
Lanaspa MA, Kuwabara M, Andres-Hernando A, Li N, Cicerchi C, Jensen T, et al. High salt intake causes leptin resistance and obesity in mice by stimulating endogenous fructose production and metabolism. Proc Natl Acad Sci USA 2018; 115(12):3138–43. doi: https://dx.doi.org/10.1073/pnas.1713837115
Gao P, You M, Li L, Zhang Q, Fang X, Wei X, et al. Salt-Induced hepatic inflammatory memory contributes to cardiovascular damage through epigenetic modulation of SIRT3. Circulation 2022; 145(5):375–91. doi: https://dx.doi.org/10.1161/CIRCULATIONAHA.121.055600
Dikalova AE, Pandey A, Xiao L, Arslanbaeva L, Sidorova T, Lopez MG, et al. Mitochondrial deacetylase Sirt3 reduces vascular dysfunction and hypertension while Sirt3 depletion in essential hypertension is linked to vascular inflammation and oxidative stress. Circ Res 2020; 126(4):439–52. doi: https://dx.doi.org/10.1161/CIRCRESAHA.119.315767
Kim A, Koo JH, Lee JM, Joo MS, Kim TH, Kim H, et al. NRF2-mediated SIRT3 induction protects hepatocytes from ER stress-induced liver injury. FASEB J 2022; 36(3):e22170. doi: https://dx.doi.org/10.1096/fj.202101470R