Mitochondrial dysfunction and vascular aging in comorbid pathology
https://doi.org/10.34215/1609-1175-2022-1-10-16
Abstract
Cardiovascular diseases take a leading position in the structure of mortality in modern society. Most diseases are characterized by uncontrolled processes of oxidative stress, proteolysis, tissue and cellular hypoxia, which cause endothelial dysfunction. Tissue and cellular hypoxia accumulated with mitochondrial reactive forms of oxygen damaging lipoproteins, proteins, nucleic acids plays an important role in the pathogenesis of vascular aging. Cellular aging is characterized by a decrease in the number of mitochondria, a decrease in the number of copies of mitochondrial DNA, and the loss of mitochondrial protein. In addition to morphological changes, the function of mitochondria is oppressed, at the same time the activity of their proteins and enzymes decreases. Changes in the functions of mitochondria can be secondary in response to various stimuli and are associated with a violation of their structure and a change in activity in response to specific genetic and phenotypic conditions. Reprogramming of mitochondrial biogenesis occupies a central position in the theory of cellular aging and is one of the targets for interventions in prolonging active longevity.
About the Authors
V. A. NevzorovaRussian Federation
Vera A. Nevzorova - MD (Medicine), PhD, Professor, Director of Institute of Therapy and Instrumental Diagnostics.
2 Ostryakova Ave. Vladivostok 690002
V. M. Chertok
Russian Federation
Victor M. Chertok - MD, PhD, professor, Head of Human Anatomy Department.
2 Ostryakova Ave., Vladivostok, 690002
T. A. Brodskaya
Russian Federation
Tatiana A. Brodskaya - MD (Medicine), PhD, Professor, Director of Department of Clinical Medicine, School of Medicine, Far Eastern FU; Professor of Institute of Therapy and Instrumental Diagnostics, Pacific SMU.
10 Ajax Bay, Russky Island, Vladivostok, 690922; 2 Ostryakova Ave. Vladivostok 690002
P. A. Selyukova
Russian Federation
Polina A. Selyukova - graduate student, Institute of Therapy and Instrumental Diagnostics.
2 Ostryakova Ave. Vladivostok 690002
N. V. Zakharchuk
Russian Federation
Natalia V. Zakharchuk - MD (Medicine), PhD, Professor of Institute of Therapy and Instrumental Diagnostics.
2 Ostryakova Ave. Vladivostok 690002
References
1. Barnett K., Mercer S.W., Norbury M., Watt G., Wyke S., Guthrie B. Epidemiology of multimorbidity and implications for health care, research, and medical education: a cross-sectional study. Lancet. 2012; 380: 37–43. DOI: 10.1016/S0140-6736(12)60240-2
2. Harris R.E., ed. Epidemiology of Chronic Diease Global Perspectives. Massachusetts, Jones and Bartlett Learning. 2013.
3. Dodds C. Physiology of ageing. Anaesth Intensive Care Med. 2006; 7: 456–458. DOI: 10.1053/j.mpaic.2006.09.011
4. Nevzorova V., Brodskaya T., Gilifanov E. Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms. Respiratory Diseases. 2020. DOI: 10.5772/intechopen.85927
5. Chertok V.M., Nevzorova V.A., Savchenko A.K., Miroshnichenko O.V., Laryushkina A.V. Age-related features of the organization of the microcirculatory bed of the bulbar conjunctiva. Pacific Medical Journal. 2020;3(81):57-61. (In Russ). DOI: 10.34215/1609-11752020-3-57-61
6. Kabalyk M.A., Nevzorova V.A. Molecular and Cellular Mechanisms of Osteoarthritis in Experimental Arterial Hypertension and Hyperlipidemia. Gerontology. 2021; 11(2): 145-151. DOI:10.1134/S2079057021020065
7. Seth R.B., Sun L., Ea C.K., Chen Z.J. Identification and characterization of MAVS, a mitochondrial antiviral signaling protein that activates NF-kappaB and IRF 3. Cell. 2005; 122: 669–682. DOI: 10.1016/j.cell.2005.08.012
8. Balaban R.S., Nemoto S., Finkel T. Mitochondria, oxidants, and aging. Cell. 2005; 120: 483–495. DOI: 10.1016/j.cell.2005.02.001
9. Kirkwood T.B. Understanding the odd science of aging. Cell. 2005; 120: 437–447. DOI: 10.1016/j.cell.2005.01.027
10. Ruas J.S., Siqueira-Santos E.S., Rodrigues-Silva E. & Castilho R.F. High glycolytic activity of tumor cells leads to underestimation of electron transport system capacity when mitochondrial ATP synthase is inhibited. Sci Rep. 2018; 8: 17383. DOI: 10.1038/s41598-018-35679-8
11. Shadel G.S., Horvath T.L. Mitochondrial ROS signaling in organismal homeostasis. Cell. 2015; 163: 560–569. DOI: 10.1016/j.cell.2015.10.001
12. Kang M.J., Yoon C.M., Kim B.H., Lee C.M., Zhou Y., Sauler M., Rober H., Anish D., Daniel B., Andrew P. Suppression of NLRX1 in chronic obstructive pulmonary disease. J Clin Invest. 2015; 125: 2458–2462. DOI: 10.1172/JCI71747.
13. Bhola P.D., Letai A. Mitochondria-judges and executioners of cell death sentences. Mol Cell. 2016; 61: 695–704. DOI: 10.1016/j.molcel.2016.02.019
14. Cloonan S.M., Choi A.M. Mitochondria in lung disease. J Clin Invest. 2016; 126: 809–820. DOI: 10.1172/JCI81113
15. Austin V., Crack Peter J., Bozinovski S., Miller Alyson A., Vlahos R. COPD and stroke: are systemic inflammation and oxidative stress the missing links? Clinical Science. 2016; 130(13) :1039. DOI: 10.1042/CS20160043
16. López-Otín C., Blasco M.A., Partridge L., Serrano M., Kroemer G. The hallmarks of ageing. Cell. 2013; 153:1194–1217. L√≥pez-Ot√≠n C., Blasco M.A., Partridge L., Serrano M., Kroemer G. The hallmarks of ageing. Cell. 2013; 153:1194-1217. DOI: 10.1016/j.cell.2013.05.039
17. Andersson S.G., Zomorodipour A., Andersson J.O., SicheritzPontén T., Alsmark U.C., Podowski R.M., Näslund A.K., Eriksson A.S., Winkler H.H., Kurland C.G. The genome sequence of Rickettsia prowazekii and the origin of mitochondria. Nature. 1998; 396(6707): 133-40. DOI: 10.1038/24094
18. Kurland C.G., Andersson S.G.E. Origin and Evolution of the Mitochondrial Proteome. Microbiol. Mol. Biol. Rev. 2000; 64: 786–820. DOI: 10.1128/MMBR.64.4.786-820.2000
19. Fitzpatrick D.A., Creevey C.J., McInerney J.O. Genome phylogenies indicate a meaningful alpha-proteobacterial phylogeny and support a grouping of the mitochondria with the Rickettsiales. Mol Biol Evol. 2006; 23(1): 74-85. DOI: 10.1093/molbev/msj009
20. Harman D. Aging: a theory based on free radical and radiation chemistry. J Gerontol. 1956; 11: 298–300. DOI: 10.1093/geronj/11.3.298
21. Schofield, C., Ratcliffe, P. Oxygen sensing by HIF hydroxylases. Nat Rev Mol Cell Biol. 2004; 5: 343–354. DOI: 10.1038/nrm1366
22. Hoffmann R.F., Zarrintan S., Brandenburg S.M., Kol A., de Bruin H.G., Jafari S., Dijk F., Kalicharan D., Kelders M., Gosker H.R., Ten Hacken N.H., van der Want J.J., van Oosterhout A.J., Heijink I.H. Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells. Respir Res. 2013; 14(1): 97. DOI: 10.1186/1465-9921-14-97
23. Nevzorova VA, Zaharchuk NV, Agafonova IG, Sarafanova NS. Features of arterial hypertension and smoking-related cerebrovascular dysfunction. Pacific Medical Journal. 2013; 4: 9–16 (In Russ).
24. Zakharchuk NV, Nevzorova VA, Chertok VM, Sarafanova NS. Effects of chronic tabacco smoking on the cerebral blood flow. Zh Nevrol Psikhiatr Im SS Korsakova. 2017;117(2):124–9 (In Russ). DOI: 10.17116/jnevro201711721124-129
25. Zaharchuk N.V., Nevzorova V.A., Chertok V.M., Roshchenko R.V. Effects of tobacco smoke on the number of HIF-1αimmunopositive neurons and capilaries in the rat brain cortex. Morphology. 2019;155(2):118 (In Russ).
26. Nevzorova V.A., Chertok V.M., Zaharchuk N.V., Chertok A.G. Effects of hypoxia on the content of hif-2α-immunopositive neurons and capillaries in rat cerebral cortex. Morphology. 2018;153(3):196-197 (In Russ).
27. Zaharchuk N.V., Chertok V.M., Nevzorova V.A., Chertok A.G. Immunocytochemical study of gelatinases and their tissue inhibitors in brain capillaries in normo- and hypertensive rats. Morphology. 2018;154(5):31-38 (In Russ).
28. Chertok V.M., Chertok A.G., Zakharchuk N.V., Nevzorova V.A. The distribution of matrix metalloproteinases and their tissue inhibitors in the brain vascular bed exposed to chronic tobacco smoke. Zh Nevrol Psikhiatr Im SS Korsakova. 2018;118(6):65-71 (In Russ).]. DOI: 10.17116/jnevro20181186165
29. Chertok V.M., Chertok A.G., Zakharchuk N.V., Nevzorova V.A. Dynamics of distribution of capillaries with matrix metalloproteinase-2 and its tissue inhibitor in rat brain during development of experimental hypertension. Bulletin of Experimental Biology and Medicine. 2018;164(3):397-401.
30. Larry H. Bernstein. The Role of Mitochondrial Imbalance in Pulmonary Diseases. EC Pulmonology and Respiratory Medicine 2019; 8.4: 336-344.
31. Parola M., Robino G., Hepa J. Oxidative stress_related molecules and liver fibrosis. J Hepatol. 2001; 35(2): 297–306. DOI: 10.1016/s0168-8278(01)00142-8
32. Giordano F.J., Oxygen, oxidative stress, hypoxia, and heart failure. J. Clin. Invest. 2005;115:500–508. DOI: 10.1172/JCI24408
33. Parekh A.K., Barton M.B. The challenge of multiple comorbidity for the US health care system. The Journal of the American Medical Association. 2010;303(13):1303–1304. DOI: 10.1001/jama.2010.381
34. Speakman J.R., Selman C. The free-radical damage theory: accumulating evidence against the simple link of oxidative stress to ageing and life span. Bioessays. 2011;33:255–259. DOI: 10.1002/bies.201000132
35. Liochev S.I. Reflections on the theories of aging, of oxidative stress, and of science in general. Is it time to abandon the free radical (oxidative stress) theory of aging? Antioxid Redox Signal 2014. [In press DOI: 10.1089/ars.2014.5928].
36. Toyama EQ, Herzig S, Courchet J, Lewis T.J., Jr., Losón O.C., Hellberg K., Young N.P., Chen H., Polleux F., Chan D.C., Reuben J. Shaw. Metabolism. AMP-activated protein kinase mediates mitochondrial fission in response to energy stress. Science 2016;351:275–28. DOI: 10.1126/science.aab4138
37. Mishra P, Chan DC. Mitochondrial dynamics and inheritance during cell division, development and disease. Nat Rev Mol Cell Biol 2014;15:634-646. DOI: 10.1038/nrm3877
38. Mizumura K, Cloonan SM, Nakahira K, Bhashyam A.R., Cervo M., Kitada T., Glass K., Owen C.A., Mahmood A., Washko G.R., Hashimoto S., Ryter S.W., Choi A.M.K. Mitophagy-dependent necroptosis contributes to the pathogenesis of COPD. J Clin Invest 2014;124:3987–4003. DOI: 10.1172/JCI74985
39. Chertok V.M., Chertok A.G., Zakharchuk N.V., Nevzorova V.A. Dynamics of distribution of capillaries with matrix metalloproteinase-2 and its tissue inhibitor in rat brain during development of experimental hypertension. Bulletin of Experimental Biology and Medicine. 2018;164(3):397-401. DOI: 10.1007/s10517-018-3998-9
40. Jackson M.V., Morrison T.J., Doherty D.F., McAuley D.F., Matthay M.A., Kissenpfennig A., Krasnodembskaya A.D. Mitochondrial transfer via tunneling nanotubes is an important mechanism by which mesenchymal stem cells enhance macrophage phagocytosis in the in vitro and in vivo models of ARDS. Stem Cells. 2016;34:2210–2223. DOI: 10.1002/stem.2372
41. Finkel T., Deng C.X., Mostoslavsky R. Recent progress in the biology and physiology of sirtuins. Nature. 2009;460:587–591. DOI: 10.1038/nature08197
42. Hoffmann R.F., Zarrintan S., Brandenburg S.M., Kol A., de Bruin H.G., Jafari S., Dijk F., Kalicharan D., Kelders M., Gosker H.R., Ten Hacken N.H., van der Want J.J., van Oosterhout A.J., Heijink I.H. Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells. Respir Res. 2013;14(1):97. DOI: 10.1186/1465-9921-14-97.
43. Wu G., Zhu Q., Zeng J., Gu X., Miao Y., Xu W., Lv T., Song. Extracellular mitochondrial DNA promote NLRP3 inflammasome activation and induce acute lung injury through TLR9 and NF-κB. J Thorac Dis 2019;11:4816–4828. DOI: 10.21037/jtd.2019.10.26
44. Gurung P., Lukens J.R., Kanneganti T.D. Mitochondria: diversity in the regulation of the NLRP3 inflammasome Trends Mol. Med., (2015;21(3):193-201. DOI: 10.1016/j.molmed.2014.11.008
45. Guimaraes C.A., Linder R. Programmed cell death: apoptosis and alternative deathstyles. Eur. J. Biochem. 2004;217:1638–1650. DOI: 10.1111/j.1432-1033.2004.04084.x
46. Harman D. Free radical theory of aging: an update: increasing the functional life span. Ann N Y Acad Sci. 2006;1067:10–21. DOI: 10.1196/annals.1354.003
47. Kovarova M., Hesker P.R., Jania L., Nguyen M.T., Snouwaert J.N., Xiang Z., Lommatzsch S.E. NLRP1-dependent pyroptosis leads to acute lung injury and morbidity in mice. J Immunol. 2012;189:2006–2016. DOI: 10.4049/jimmunol. 1201065
48. Mora A.L., Rojas M. Adult stem cells for chronic lung diseases. Respirology. 2013;18:1041-1046. DOI: 10.1111/resp.12112
49. Rashida Gnanaprakasam J.N., Wu R., Wang R. Metabolic reprogramming in modulating T cell reactive oxygen species generation and antioxidant capacity. Front. Immunol. 2018;9:1075. DOI: 10.3389/fimmu.2018.01075
50. Kamiński M.M., Röth D., Krammer P.H., Gülow K. Mitochondria as oxidative signaling organelles in T-cell activation: physiological role and pathological implications. Arch Immunol Ther Exp (Warsz). 2013;61(5):367-384. DOI: 10.1007/s00005013-0235-0
51. Virmani R., Avolio A.P., Mergner W.J., Robinowitz M., Herderick E.E., Cornhill J.F. Effect of aging on aortic morphology in populations with high and low prevalence of hypertension and atherosclerosis: comparison between occidental and Chinese communities. Am J Pathol. 1991;139:1119–1129.
52. Robert L. Aging of the vascular wall and atherogenesis: role of the elastini-laminin receptor. Atherosclerosis. 1996;123:169–179. DOI: 10.1016/0021-9150(96)05804-2
53. Tennant D.A., Durán R.V., Gottlieb E. Targeting metabolic transformation for cancer therapy. Nat Rev Cancer. 2010;10:267–277. DOI: 10.1038/nrc2817
54. de Cabo R., Carmona-Gutierrez D., Bernier M., Hall M.N., Madeo F. The search for antiaging interventions: from elixirs to fasting regimens. Cell. 2014;157:1515–1526. DOI: 10.1016/j.cell.2014.05.031
Review
For citations:
Nevzorova V.A., Chertok V.M., Brodskaya T.A., Selyukova P.A., Zakharchuk N.V. Mitochondrial dysfunction and vascular aging in comorbid pathology. Pacific Medical Journal. 2022;(1):10-16. (In Russ.) https://doi.org/10.34215/1609-1175-2022-1-10-16