The Optimal Coexistence of Cells: How Could Human Cells Create The Integrative Physiology

Rafik D. Grygoryan (Institute of software systems in Cybernetics center of NAS)

Article ID: 1386

Abstract


A general view of human physiology is proposed. Each of 220 cell types must provide its intimate functions despite occasional or chronic obstacles created by other cells. The physiological mechanisms are independently emerged and evolutionarily saved due to their ability to provide optimal-like coexistence of cells on a background of destructive challenges of external/internal environments. In certain limits, both cells and organs are adaptive. The cell has accumulated both passive adaptation mechanisms mainly parallel working in the biochemistry, and active physiological mechanisms fighting for the optimal cell metabolism. Its rate depends on the cell type and current phase into the cell cycle. The adaptive properties of organs and their functional systems have resulted from the cells’ adaptivity. The impaired cells (under energy lack and/or contaminated cytoplasm) produce adaptation factors acting both in the cell and at multiple organism-scales. Multicellular mechanisms, enhancing the cell fight for energy balance, creating the due cytoplasm for optimizing metabolism, force the most physiological characteristics, including the mean arterial pressure to fluctuate or shift. The view is a basis for re-thinking the concept of the so-called physiological norm and fundamental mechanisms of age-associated pathologies, in particular, hypertension.


Keywords


Cell metabolism; Energy shortage; Cytoplasm purifiers; Adaptation; Functional systems; Hypertension

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References


[1] Cymerman A. The Physiology of High-Altitude Exposure. In: Nutritional Needs in Cold and High-Altitude Environments. Ed-s. Marriott B.M., Carlson S.J.,1996, Institute of Medicine. Committee on Military Nutrition Research.

[2] Weber R.E. High-altitude adaptations in vertebrate hemoglobins. Respiratory Physiology & Neurobiology. 2007, 158:132–142.

[3] http://dx.doi.org:/10.1016/j.resp.2007.05.001

[4] Hainsworth R, Drinkhill MJ. Cardiovascular adjustments for life at high altitude. Respir. Physiol. Neurobiol. 2007, 158(2-3): 204–211.

[5] Rimoldi SF, Sartori C, Seiler C, Delacretaz E, Mattle HP, Scherrer U, et al. High-altitude exposure in patients with cardiovascular disease: risk assessment and practical recommendations. Prog Cardiovasc Dis. 2010, 52(6): 512–524.

[6] Grygoryan RD, Lissov PN, Aksenova TV, Moroz AG. The specialized software-modeling complex “PhysiolResp”. Problems of programming, 2009, 2: 140-150 (Rus).

[7] Grygoryan RD, Hargens AR. A virtual multicellular organism with homeostatic and adaptive properties. In: Adaptation Biology and Medicine: Health Potentials. Ed. L. Lukyanova, N.Takeda, P.K. Singal. – New Delhi: Narosa Publishing House, 2008, 5: 261 –282.

[8] Convertino V, Hoffler GW. Cardiovascular physiology. Effects of microgravity. J Fla Med Assoc, 1992, 79(8): 517-524.

[9] Hargens AR, Watenpaugh DE. Cardiovascular adaptation to spaceflight. Med Sci Sports Exerc, 1996, 28(8): 977-982.

[10] Buckey JC Jr1, Gaffney FA, Lane LD, Levine BD, Watenpaugh DE, Wright SJ, Yancy CW Jr, Meyer DM, Blomqvist CG. Central venous pressure in space. J Appl Physiol, 1996, 81 (1): 19-25.

[11] Grygoryan RD. Self-organization of homeostasis and adaptation. Кiev, Academperiodics, 2004: 502. (Rus.).

[12] ISBN: 966-8002-99-7

[13] Grygoryan RD. The biodynamics and models of energy stress. Кiev, Academperiodics, 2012: 330. (Rus.).

[14] ISBN: 978-966-02-5393-3

[15] Grygoryan RD. The Energy basis of reversible adaptation. N.Y.: Nova Science, 2012: 254.

[16] ISBN: 978-1-62081-093-4

[17] Grygoryan RD. An individual physiological norm: the concept and problems. Reports of the National Academy of Sciences of Ukraine, 2013, 8: 156-162 (Rus.).

[18] Grygoryan RD, Lyabakh KG. Arterial pressure: comprehension. Кiev, Academperiodics, 2015, 458с (Rus.).

[19] ISBN: 978-966-02-7781-6

[20] Grygoryan RD. The optimal circulation: cells contribution to arterial pressure. N.Y.: Nova Science, 2017: 287.

[21] ISBN: 978-1-53612-295-4

[22] Grygoryan RD, Sagach VF. The concept of physiological super-systems: New stage of integrative physiology. Int. J. Physiol. and Pathophysiology, 2018, 9(2): 169-180.

[23] Grygoryan RD. Comprehension of individual adaptation mechanisms: endogenous tuning of constants determining optimal physiological states. Slovak int. scientific j., 2019, 32: 67-72.

[24] Grygoryan RD. Principles of multicellular physiological systems. Slovak int. scientific j, 2019, 33: 45-50.

[25] Grygoryan R.D. The unknown aspects of arterial pressure. Znanstvena misel journal, 2019, 33: 19-23.

[26] Grygoryan RD. Principles of the multicellularity: a view from inside. Znanstvena misel journal, 2019, 34: 48-53.

[27] Cannon WB. Organization for physiological homeostasis. Physiol 1929, 9: 399–431.

[28] Woods HA, Wilson JK. An information hypothesis for the evolution of homeostasis. Trends Ecol Evol, 2013, 28: 283–289. [PubMed] [Google Scholar]

[29] Modell H, Cliff W, Michael J, McFarland J, Wenderoth MP, Wright A. A physiologist’s view of homeostasis. Adv Physiol Educ. 2015, 39(4): 259-266.

[30] DOI: 10.1152/advan.00107.2015

[31] Lopez-Gambero AJ, Salazar K, Martínez F, Cifuentes M, Nualart F. Brain glucose-sensing mechanism and energy homeostasis. Molecular Neurobiology, 2018, 56(14).

[32] DOI: 10.1007/s12035-018-1099-4

[33] McEwen BS. Central Role of the Brain in Stress and Adaptation. In Stress: Concepts, Cognition, Emotion, and Behavior, Handbook in Stress Series, V. 1, Ed. By G. Fink, Academic Press, 2016.

[34] Lester BM, Conradt E, Marsit C. Introduction to the Special Section on Epigenetics. Child Dev. 2016, 87(1): 29–37.

[35] DOI: 10.1111/cdev.12489

[36] Liang M. Epigenetic Mechanisms and Hypertension. Hypertension. 2018, 72: 1244–1254.

[37] https://doi.org/10.1161/HYPERTENSIONAHA.118.11171

[38] Korkmaz A, Manchester LC, Topal T, Ma S, Tan DX, Reiter RG. Epigenetic mechanisms in human physiology and diseases. Journal of Experimental and Integrative Medicine. 2011, 1(3): 139-147.

[39] DOI: 10.5455/jeim.060611.rw.003

[40] Lacal I, Ventura R. Epigenetic Inheritance: Concepts, Mechanisms and Perspectives. Front Mol Neurosci. 2018, 11: 292.

[41] DOI: 10.3389/fnmol.2018.00292

[42] Meerson FZ. Adaptation, stress and prophylaxis. Springer, 1984.

[43] Hardie DG, Ashford ML. AMPK: regulating energy balance at the cellular and whole body level. Physiology (Bethesda). 2014, 29(2): 99–107.

[44] Chance B, Leigh J, Kent J, McCully K. Metabolic control principles and P31NMR. Federation Proc.,1986, 45: 2915-2920.

[45] Pan Y, Mansfield KD, Bertozzi CC, Rudenko V, Chan DA, Giaccia AJ, et al. Multiple factors affecting cellular redox status and energy metabolism modulate hypoxia-inducible factor prolyl hydroxylase activity in vivo and in vitro. Mol Cell Biol. 2007, 27: 912–925.

[46] DOI: 10.1128/MCB.01223-06

[47] Grygoryan RD. The relativity concept for human physiology and health assessment. Slovak Int. Scientific J, 2019,34: 45-50.

[48] Guyton AC, Coleman TG, Granger HJ. Circulation: overall regulation. Annu.Rev. Physiol., 1972, 34: 13-46.

[49] Sparks MA, Crowley SD, Gurley SB, Mirotsou M, Coffman TM. Classical Renin-Angiotensin system in kidney physiology. Compr Physiol. 2014, 4(3): 1201–1228.

[50] DOI: 10.1002/cphy.c130040

[51] Guyton AC. Blood pressure control - special role of the kidneys and body fluids. Science. 1991, 252: 1813–1816.

[52] Montani J-P, Van Vliet BN. Understanding the contribution of Guyton’s large circulatory model to long-term control of arterial pressure. Exp Physiol. 2009, 94: 382–388.

[53] Cowley AW Jr. Long-term control of arterial pressure. Physiol Rev. 1992, 72: 231-300.

[54] Cowley AW Jr. Renal medullary oxidative stress, pressure-natriuresis, and hypertension. Hypertension. 2008, 52: 777–786.

[55] Semenza G L, Wang G L. A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation. Mol Cell Biol. 1992, 12(12): 5447–5454.

[56] Rey S, Semenza GL. Hypoxia-inducible factor-1-dependent mechanisms of vascularization and vascular remodelling. Cardiovasc Res. 2010, 86(2): 236-42. Epub 2010 Feb 17.

[57] Dengler VL, Galbraith M, Espinosa JM. Transcriptional regulation by hypoxia inducible factors. Crit Rev Biochem Mol Biol.2014, 49: 1–15.

[58] DOI: 10.3109/10409238.2013.838205

[59] Semenza GL. Hypoxia-inducible factors: coupling glucose metabolism and redox regulation with induction of the breast cancer stem cell phenotype. EMBO J. 2017, 36: 252 – 259.

[60] DOI: 10.15252/embj.201695204

[61] Schofield CJ, Ratcliffe PJ. Oxygen sensing by HIF hydroxylases. Nat Rev Mol Cell Biol. 2004, 5(5): 343-54.

[62] DOI: 10.1038/nrm1366

[63] Chistiakov DA, Shkurat TP, Melnichenko AA, Grechko AV, Orekhov AN. The role of mitochondrial dysfunction in cardiovascular disease: a brief review. Ann Med. 2018, 50(2): 121-127.

[64] DOI: 10.1080/07853890.2017.1417631

[65] Cheng J, Nanayakkara G, Shao Y, Cueto R, Wang L, Yang WY, Tian Y, Wang H, Yang X. Mitochondrial Proton Leak Plays a Critical Role in Pathogenesis of Cardiovascular Diseases. Exp Med Biol. 2017, 982: 359-370.

[66] DOI: 10.1007/978-3-319-55330-6_20

[67] Grünewald A, Kumar KR, Sue CM. New insights into the complex role of mitochondria in Parkinson’s disease. Progress in Neurobiology.2019, 177: 73-93.

[68] DOI: org/10.1016/j.pneurobio.2018.09.003

[69] Farag E, Maheshwari K, Morgan J, Sakr Esa WA, Doyle DJ. An update of the role of renin angiotensin in cardiovascular homeostasis. Anesth Analg. 2015, 120(2): 275–292.

[70] Briones AM,Toyus R. Oxidative Stress and Hypertension: Current Concepts. Current Hypertension Reports, 2010, 12(2): 135-142.

[71] DOI: 10.1007/s11906-010-0100-z

[72] Fogg VC, Lanning NJ, Mackeigan M. Mitochondria in cancer: at the crossroads of life and death. JP. Chin J Cancer. 2011, 30(8): 526-39.

[73] DOI: 10.5732/cjc.011.10018

[74] Lee HC, Huang KH, Yeh TS, Chi CW. Somatic alterations in mitochondrial DNA and mitochondrial dysfunction in gastric cancer progression. World J Gastroenterol. 2014, 20(14): 3950-9.

[75] DOI: 10.3748/wjg.v20.i14.3950

[76] Sajnani K, Islam F, Smith RA, Gopalan V, Lam AK. Genetic alterations in Krebs cycle and its impact on cancer pathogenesis. Biochimie.2017, 135: 164-172.

[77] DOI: 10.1016/j.biochi.2017.02.008

[78] Lee RG, Sedghi M, Salari M, Shearwood AMJ, Stentenbach M, Kariminejad A, Goullee H, Rackham O, Laing NG, Tajsharghi H, Filipovska A. Early-onset Parkinson disease caused by a mutation in CHCHD2 and mitochondrial dysfunction. Neurol Genet, 2018, 4.

[79] DOI: 10.1212/NXG.0000000000000276

[80] Larsen, S.B., Hanss, Z. & Krüger, R. The genetic architecture of mitochondrial dysfunction in Parkinson’s disease. Cell Tissue Res. 2018, 373 (1): 21–37.

[81] https://doi.org/10.1007/s00441-017-2768-8

[82] Anilkumar U, Weisová P, Düssmann H, Concannon CG, König HG, Prehn JHM. AMP-activated protein kinase (AMPK)-induced preconditioning in primary cortical neurons involves activation of MCL-1. J. Neurochem. 2013. 124, 721–734.

[83] DOI: 10.1111/jnc.12108

[84] Jeon SM. Regulation and function of AMPK in physiology and diseases. Exp Mol Med. 2016, 48(7): e245.

[85] DOI: 10.1038/emm.2016.81

[86] Dasgupta B, Chhipa RR. Evolving lessons on the complex role of AMPK in normal physiology and cancer. Trends Pharmacol Sci. 2016, 37(3): 192-206.

[87] Hardie GH. Keeping the home fires burning: AMP-activated protein kinase. J. R. Soc. Interface. 2018, 15: 20170774.

[88] http://dx.doi.org/10.1098/rsif.2017.0774

[89] Fiala D, Psikuta A, Jendritsky G, et al. Physiological modeling for technical, clinical and research applications. Frontiers in bioscience (Scholar edition). 2010, 2(3): 939-968.

[90] DOI: 10.2741/S112

[91] Olsen HC, Ottesen JT, Smith R, Olufsen M. Parameter subset selection techniques for problems in mathematical biology. Biological Cybernetics. 2018, 113(6).

[92] DOI: 10.1007/s00422-018-0784-8

[93] Hester RL, Iliescu R, Summers R, Coleman TG. Systems biology and integrative physiological modeling. J Physiol. 2011, 589(5): 1053–1060.

[94] DOI: 10.1113/jphysiol.2010.201558

[95] Jazek F., Kulhanek T., Konfranek J. Lumped models of the cardiovascular system of various complexity. Biocybernetics and Biomedical Engineering, 2017, 37(4).

[96] Grygoryan RD, Aksionova TV, Degoda AG. A computer simulator of mechanisms providing energy balance in human cells. Cybernetics and computer engineering, 2017, 184: 72-83. (Rus.).

[97] Grygoryan RD, Degoda AG, Dzhurinsky EA, Aksenova TV. A simulator of human physiology under energy balance in cells. Рroblems in programming, 2019, 4: 93-100.

[98] Lohmeier TE, Iliescu R. The Baroreflex as a Long-Term Controller of Arterial Pressure. Physiology (Bethesda). 2015, 30(2): 148–158.

[99] DOI: 10.1152/physiol.00035.2014.

[100] Cross MJ, Claesson-Welsh L. FGF and VEGF function in angiogenesis: Signalling pathways, biological responses and therapeutic inhibition. Trends Pharmacol. Sci. 2001, 22: 201–207.

[101] DOI: 10.1016/S0165-6147(00)01676-X

[102] Thangarajah H, Yao D, Chang EI et al., The molecular basis for impaired hypoxia-induced VEGF expression in diabetic tissues. Proc. Nat. Acad. Sci. USA, 2009, 106( 32): 13505–13510.

[103] Maechler P, Carobbio S, Rubi B. In beta-cells, mitochondria integrate and generate metabolic signals controlling insulin secretion. Intern. J Biochem. Cell Biol., 2010, 38: 696-709.

[104] Caporarello N, Meridew JA, Jones DL, Tan Q, Haak AJ, Choi KM, Manlove LJ, Prakash YS, Tschumperlin DJ. Ligresti G. PGC1alpha repression in IPF fibroblasts drives a pathologic metabolic, secretory and fibrogenic state. Thorax. 2019, 74(8): 749-760.

[105] DOI: 10.1136/thoraxjnl-2019-213064

[106] Otrock ZK, Mahfouz RA, Makarem JA, Shamseddine AI. Understanding the biology of angiogenesis: review of the most important molecular mechanisms. Blood Cells Mol Dis. 2007, 39(2): 212-220.

[107] De Mello WC, Frohlich ED. On the local cardiac renin angiotensin system. Basic and clinical implications. Peptides. 2011, 32: 1774–1779.

[108] Ho TK, Abraham DJ, Black CM, Baker DM. Hypoxia-inducible factor 1 in lower limb ischemia. Vascular. 2006, 14(6): 321-327.

[109] Minet E, Michel G, Remacle J, Michiels C. Role of HIF-1 as a transcription factor involved in embryonic development, cancer progression and apoptosis (review). Int J Mol Med, 2000, 5: 253–9.

[110] DOI: 10.3892/ijmm.5.3.253

[111] Yoon D, Ponka P, Prchal JT. Hypoxia and hematopoiesis. Am. J.Physiol.-Cell Physiol., 2011, 300 (6): C1215–C1222.

[112] Adach W, Olas B. Carbon monoxide and its donors - their implications for medicine. Future Med Chem. 2019, 11(1): 61-73.

[113] Semenza GL. Involvement of oxygen-sensing pathways in physiologic and pathologic erythropoiesis. Blood J., 2009, 114(10): 1-27.

[114] Efremov RG, Baradaran R, Sazanov LA. The architecture of respiratory complex I. Nature, 2010, 465: 441-445.

[115] Beard D, Muriel M. Mechanisms of pressure-diuresis and pressure-natriuresis in Dahl salt-resistant and Dahl salt-sensitive rats. BMC Physiology, 2012, 12(1): 6.

[116] DOI: 10.1186/1472-6793-12-6

[117] Ivy JR, Bailey MA. Pressure natriuresis and the renal control of arterial blood pressure. J. of physiol., 2014, 592(18): 3955-3967.

[118] https://doi.org/10.1113/jphysiol.2014.271676

[119] Braganza A, Corey CG, Santanasto AJ, Distefano G, Coen PM, Glynn NW, Nouraie SM, Goodpaster BH, Newman AB. Shiva S. Platelet bioenergetics correlate with muscle energetics and are altered in older adults. JCI Insight. 2019, 23: 5.

[120] DOI: 10.1172/jci.insight.128248

[121] Chan CM, Huang DY, Sekar P, Hsu SH. Lyin WW. Reactive oxygen species-dependent mitochondrial dynamics and autophagy confer protective effects in retinal pigment epithelial cells against sodium iodate-induced cell death. J Biomed Sci. 2019; 26(1):40.

[122] DOI: 10.1186/s12929-019-0531-z

[123] Malińska D, Więckowski MR, Michalska B, Drabik K, Prill M, Patalas-Krawczyk P, Walczak J, Szymański J, Mathis C, Van der Toorn M, et al. Mitochondria as a possible target for nicotine action. J Bioenerg Biomembr. 2019, 51(4): 259-276.

[124] DOI: org/10.1007/s10863-019-09800-z

[125] Salin K, Rey B, Selman C, Metcalfe NB. Variation in the link between oxygen consumption and ATP production, and its relevance for animal performance. Proceedings of the Royal Society B, 2015, 282(1812).

[126] https://doi.org/10.1098/rspb.2015.1028

[127] Zucker HI, Xiao L, Haack KKV. The Central RAS and Sympathetic Nerve Activity in Chronic Heart Failure. Clin Sci (Lond), 2014, 126(10): 695–706.

[128] DOI: 10.1042/CS20130294

[129] Grygoryan RD, Aksenova TV, Degoda AG. A simulator of mechanisms providing energy balance in human cells. Cybernetics and Comput. Technologies. 2017, 2: 67–76.

[130] Lee JW, Ko J, Ju C, Eltzschig HK.Hypoxia signaling in human diseases and therapeutic targets. Exp Mol Med. 2019, 51(6): 68.

[131] DOI: 10.1038/s12276-019-0235-1

[132] Mesarwi OA, Shin MK, Bevans-Fonti S, Schlesinger C, Shaw J, Polotsky VY. Hepatocyte Hypoxia Inducible Factor-1 Mediates the Development of Liver Fibrosis in a Mouse Model of Nonalcoholic Fatty Liver Disease. PLoS One. 2016, 11(12): e0168572.

[133] DOI: 10.1371/journal.pone.0168572

[134] Menendez-Montes, Escobar B, Palacios B, Gómez MJ et al., 2016, Developmental Cell 39: 724–739.

[135] http://dx.doi.org/10.1016/j.devcel.2016.11.012



DOI: https://doi.org/10.30564/jhp.v1i1.1386

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