Interaction of the neuroendocrine and immune mechanisms of progression of myocardial damage

Abstract


The review summarizes data on the interference of the neuroendocrine and immune mechanisms of myocardial remodeling. It shows a role of the effectors of the renin-angiotensin-aldosterone (aldosterone and angiotensin II) and sympathoadrenal (noradrenaline) systems in the activation of macrophages, the production of proinflammatory cytokines and inflammatory cell chemoattractants. It is noted that proinflammatory cytokines in turn promote the activation of these neuroendocrine systems. Natriuretic peptides exert an anti-inflammatory effect, but their production can be activated by proinflammatory cytokines.

References

  1. Гуревич М. А. Хроническая сердечная недостаточность: Руководство для врачей. 5-е изд. М.: Практическая медицина; 2008.
  2. Калюжин В. В., Калюжин О. В., Тепляков А. Т. Хроническая сердечная недостаточность: вопросы этиологии, эпидемиологии, патогенеза (гемодинамические, нейрогуморальные, иммунные, генетические аспекты), диагностики и лечения. М.: МИА; 2006.
  3. Озова Е. М., Киякбаев Г. К., Кобалава Ж. Д. Воспаление и хроническая сердечная недостаточность. Роль статинов. Кардиология 2007; 47(1): 52-64.
  4. Frangogiannis N. G. Targeting the inflammatory response in healing myocardial infarcts. Curr. Med. Chem. 2006; 13(16): 1877-1893.
  5. Zhang M., Chen L. Status of cytokines in ischemia reperfusion induced heart injury. Cardiovasc. Hematol. Disord. Drug Targets 2008; 8(3): 161-172.
  6. Mann D. L. Stress-activated cytokines and the heart: from adaptation to maladaptation. Annu. Rev. Physiol. 2003; 35: 81- 101.
  7. Баллюзек М. Ф., Гриненко Т. Н., Кветной И. М. Гормоны сердца в формировании сердечно-сосудистой патологии. Клин. мед. 2005; 83(11): 4-13.
  8. Weber K. T. A neuroendocrine-immune interface. The immunostimulatory state of aldosteronism. Herz 2003; 28(8): 692- 701.
  9. Armanini D., Zennaro C. M., Martella L. et al. Regulation of aldosterone receptor in hypertension. Steroids 1993: 58: 611- 613.
  10. Gerling I. C., Sun Y., Ahokas R. A. et al. Aldosteronism. An immunostimulatory state precedes the proinflammatory/fibrogenic cardiac phenotype. Am. J. Physiol. Heart Circ. Physiol. 2003: 285: 813-821.
  11. Ahokas R. A., Sun Y., Bhattacharya S. K. et al. Aldosteronism and a proinflammatory vascular phenotype: role of Mg2+, Ca2+, and H2O2 in peripheral blood mononuclear cells. Circulation 2005; 111(1): 51-57.
  12. Funder J. W. Aldosterone, mineralocorticoid receptors and vascular inflammation. Mol. Cell. Endocrinol. 2004; 217(1): 263-269.
  13. Armanini D., Fiore C., Calo L. A. Mononuclear leukocyte mineralocorticoid receptors. A possible link between aldosterone and atherosclerosis. Hypertension 2006; 47(2): 4.
  14. Nicoletti A., Michel J.-B. Cardiac fibrosis and inflammation: interaction with hemodynamic and hormonal factors. Cardiovasc. Res. 1999; 41(2): 532-543.
  15. Wilson P., Morgan J., Funder J. W. et al. Mediators of mineralocorticoid receptor-induced profibrotic inflammatory responses in the heart. Clin. Sci. (Lond.) 2009; 116(9): 731- 739.
  16. Neves M. F., Amiri F., Virdis A. et al. Role of aldosterone in angiotensin II-induced cardiac and aortic inflammation, fibrosis, and hypertrophy. Can. J. Physiol. Pharmacol. 2005; 83(11): 999-1006.
  17. Rocha R., Martin-Berger C. L., Yang P. et al. Selective aldosterone blockade prevents angiotensin II/salt-induced vascular inflammation in the rat heart. Endocrinology 2002; 143(12): 4828-4836.
  18. Toko H., Zou Y., Minamino T. et al. Angiotensin II type 1a receptor is involved in cell infiltration, cytokine production, and neovascularization in infarcted myocardium. Arterioscler. Thromb. Vasc. Biol. 2004; 24(4): 664-670.
  19. Mateo T., Abu Nabah Y. N., Abu Taha M. et al. Angiotensin II-induced mononuclear leukocyte interactions with arteriolar and venular endothelium are mediated by the release of different CC chemokines. J. Immunol. 2006; 176(9): 5577-5586.
  20. Kim H. Y., Kang Y. J., Song I. H. et al. Upregulation of interleukin-8/CXCL8 in vascular smooth muscle cells from spontaneously hypertensive rats. Hypertens. Res. 2008; 31(3): 515- 523.
  21. Yokoyama T., Sekiguchi K., Tanaka T. et al. Angiotensin II and mechanical stretch induce production of tumor necrosis factor in cardiac fibroblasts. Am. J. Physiol. 1999; 276(6, Pt 2): 1968-1976.
  22. Dandona P., Dhindsa S., Ghanim H., Chaudhuri A. Angiotensin II and inflammation: the effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockade. J. Hum. Hypertens. 2007; 21(1): 20-27.
  23. White M., Lepage S., Lavoie J. Effects of combined candesartan and ACE inhibitors on BNP, markers of inflammation and oxidative stress, and glucose regulation in patients with symptomatic heart failure. J. Card. Fail. 2007; 13(2): 86-94.
  24. Murakami Y., Kurosaki K., Matsui K. et al. Serum MCP-l and VEGF levels are not affected by inhibition of the renin-angiotensin system in patients with acute myocardial infarction. Cardiovasc. Drugs Ther. 2003; 17(3): 249-255.
  25. Akgul A. Can cardiac fibrosis be prevented? Mast cell inhibition versus anti-chymase activity. Eur. J. Cardiothorac. Surg. 2009; 35(3): 553-554.
  26. Bader M., Ganten D. Update on tissue renin-angiotensin systems. J. Mol. Med. 2008; 86(6): 615-621.
  27. Flesch M., Hoper A., Dell'Italia L. et al. Activation and functional significance of the renin-angiotensin system in mice with cardiac restricted overexpression of tumor necrosis factor. Circulation 2003; 108(5): 598-604.
  28. Gurantz D., Cowling R. T., Varki N. et al. IL-1beta and TNF-alpha upregulate angiotensin II type 1 (AT1) receptors on cardiac fibroblasts and are associated with increased AT1 density in the post-MI heart. J. Mol. Cell. Cardiol. 2005; 38(3): 505- 515.
  29. Peng J., Gurantz D., Tran V. et al. Tumor necrosis factor-alpha-induced AT1 receptor upregulation enhances angiotensin II-mediated cardiac fibroblast responses that favor fibrosis. Circ. Res. 2002; 91(12): 1119-1126.
  30. Murray D. R., Prabhu S. D., Chandrasekar B. Chronic beta-adrenergic stimulation induces myocardial proinflammatory cytokine expression. Circulation 2000; 101(20): 2338-2341.
  31. Neri M., Cerretani D., Fiaschi A. I. et al. Correlation between cardiac oxidative stress and myocardial pathology due to acute and chronic norepinephrine administration in rats. J. Cell. Mol. Med. 2007; 11(1): 156-170.
  32. Fu Y. C., Chi C. S., Yin S. C. et al. Norepinephrine induces apoptosis in neonatal rat cardiomyocytes through a reactive oxygen species-TNF alpha-caspase signaling pathway. Cardiovasc. Res. 2004; 62(3): 558-567.
  33. Berczi I., Quintanar-Stephano A., Kovacs K. Neuroimmune regulation in immunocompetence, acute illness, and healing. Ann. N. Y. Acad. Sci. 2009; 1153: 220-239.
  34. Guggilam A., Haque M., Kerut E. K. et al. TNF-alpha blockade decreases oxidative stress in the paraventricular nucleus and attenuates sympathoexcitation in heart failure rats. Am. J. Physiol. Heart Circ. Physiol. 2007; 293(1): 599-609.
  35. Reithmann C., Gierschik P., Jakobs K. H., Werdan K. Regulation of adenylyl cyclase by noradrenaline and tumour necrosis factor alpha in rat cardiomyocytes. Eur. Heart J. 1991; 12(Suppl. F): 139-142.
  36. Matsuo H. Discovery of a natriuretic peptide family and their clinical application. Can. J. Physiol. Pharmacol. 2001; 79(8): 736-740.
  37. Vollmar A. M., Schulz R. Expression and differential regulation of natriuretic peptides in mouse macrophages. J. Clin. Invest. 1995; 95(6): 2442-2450.
  38. Vollmar A. M. The role of atrial natriuretic peptide in the immune system. Peptids 2005; 26(6): 1086-1094.
  39. Kiemer A. K., Vollmar A. M. Autocrine regulation of inducible nitric oxide synthase in macrophages by atrial natriuretic peptide. J. Biol. Chem. 1998; 273: 13444-13451.
  40. Kiemer A. K., Vollmar A. M. Elevation of intracellular calcium levels contributes to the inhibition of inducible nitric oxide synthase by atrial natriuretic peptide. Immunol. Cell. Biol. 2001; 79(1): 11-17.
  41. Kiemer A. K., Lehner M. D., Hertung T., Vollmar A. M. Inhibition of cyclooxygenase-2 by natriuretic peptides. Endocrinology 2002; 143(3): 846-852.
  42. Kiemer A. K., Hartung T., Vollmar A. M. cGMP-mediated inhibition of TNF-alpha production by the atrial natriuretic peptide in murine macrophages. J. Immunol. 2000; 165: 175-181.
  43. Kiemer A. K., Vollmar A. M. The atrial natriuretic peptide regulates the production of inflammatory mediators in macrophages. Ann. Rheum. Dis. 2001; 60(Suppl. 3): 68-70.
  44. Ma K. K., Ogawa T., de Bold A. J. Selective upregulation of cardiac brain natriuretic peptide at the transcriptional and translational levels by proinflammatory cytokines and by conditioned medium derived from mixed lymphocyte reactions via p38 MAP kinase. J. Mol. Cell. Cardiol. 2004; 36(4): 505-513.
  45. Kapoun A. M., Liang F., O'Young G. et al. B-type natriuretic peptide exerts broad functional opposition to transforming growth factor-beta in primary human cardiac fibroblasts: fibrosis, myofibroblast conversion, proliferation, and inflammation. Circ. Res. 2004; 94(4): 453-461.

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Copyright (c) 2020 Krasnosel'skiy M.Y., Vorob'ev P.A., Tsurko V.V., Krasnoselsky M.Y., Vorobyev P.A., Tsurko V.V.

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