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肌肉组织中线粒体功能损伤在脓毒症诱发脏器功能障碍研究进展
Research Progress of Mitochondrial Function Impairment in Muscle Tissue in Organ Dysfunction Induced by Sepsis

DOI: 10.12677/ACM.2023.13112559, PP. 18242-18248

Keywords: 脓毒症,线粒体,肌肉组织
Sepsis
, Mitochondria, Muscle Tissue

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Abstract:

脓毒症是重症监护室(ICU)最常见的疾病,其主要特征是多脏器功能障碍,而线粒体损伤引发的器官功能障碍是脓毒症的主要并发症。线粒体通过产生三磷酸腺苷(ATP)为机体的各种代谢的关键步骤提供能量。肌肉组织中的细胞内含有大量线粒体,氧化磷酸化异常可能损害ATP的生成,导致生物能量不足,细胞受损,诱发脓毒症性器官功能障碍。
Sepsis is the most common disease in intensive care unit (ICU), which is characterized by multiple organ dysfunction, and organ dysfunction caused by mitochondrial damage is the main complica-tion of sepsis. Mitochondria produce adenosine triphosphate (ATP) to provide energy for various key metabolic steps in the body. There are a large number of mitochondria in the cells of muscle tissue. Abnormal oxidative phosphorylation may damage ATP generation, lead to bioenergy defi-ciency, cell damage, and induce septic organ dysfunction.

References

[1]  Vincent, J.L., Jones, G., David, S., Olariu, E. and Cadwell, K.K. (2019) Frequency and Mortality of Septic Shock in Eu-rope and North America: A Systematic Review and Meta-Analysis. Critical Care, 23, Article No. 196.
https://doi.org/10.1186/s13054-019-2478-6
[2]  Eyenga, P., Rey, B., Eyenga, L., et al. (2022) Regulation of Oxi-dative Phosphorylation of Liver Mitochondria in Sepsis. Cells, 11, Article 1598.
https://doi.org/10.3390/cells11101598
[3]  Mokhtari, B., Hamidi, M., Badalzadeh, R. and Mahmoodpoor, A. (2023) Mitochondrial Transplantation Protects against Sepsis-Induced Myocardial Dysfunction by Modulating Mito-chondrial Biogenesis and Fission/Fusion and Inflammatory Response. Molecular Biology Reports, 50, 2147-2158.
https://doi.org/10.1007/s11033-022-08115-4
[4]  Singer, M. (2014) The Role of Mitochondrial Dysfunction in Sepsis-Induced Multi-Organ Failure. Virulence, 5, 66-72.
https://doi.org/10.4161/viru.26907
[5]  Murphy, E., Ardehali, H., Balaban, R.S., et al. (2016) Mitochondrial Func-tion, Biology, and Role in Disease: A Scientific Statement from the American Heart Association. Circulation Research, 118, 1960-1991.
https://doi.org/10.1161/RES.0000000000000104
[6]  Antonucci, E., Fiaccadori, E., Donadello, K., et al. (2014) Myocardial Depression in Sepsis: From Pathogenesis to Clinical Manifestations and Treatment. Journal of Critical Care, 29, 500-511.
https://doi.org/10.1016/j.jcrc.2014.03.028
[7]  Brown, D.A., Perry, J.B., Allen, M.E., et al. (2017) Expert Con-sensus Document: Mitochondrial Function as a Therapeutic Target in Heart Failure. Nature Reviews Cardiology, 14, 238-250.
https://doi.org/10.1038/nrcardio.2016.203
[8]  Barth, E., St?mmler, G., Speiser, B. and Schaper, J. (1992) Ultra-structural Quantitation of Mitochondria and Myofilaments in Cardiac Muscle from 10 Different Animal Species Including Man. Journal of Molecular and Cellular Cardiology, 24, 669-681.
https://doi.org/10.1016/0022-2828(92)93381-S
[9]  Fukumoto, K., Pierro, A., Spitz, L. and Eaton S., (2003) Car-diac and Renal Mitochondria Respond Differently to Hydrogen Peroxide in Suckling Rats. Journal of Surgical Research, 113, 146-150.
https://doi.org/10.1016/S0022-4804(03)00233-6
[10]  Kozlov, A.V., Staniek, K., Haindl, S., et al. (2006) Different Effects of Endotoxic Shock on the Respiratory Function of Liver and Heart Mitochondria in Rats. American Journal of Physiology-Gastrointestinal and Liver Physiology, 290, G543-F549.
https://doi.org/10.1152/ajpgi.00331.2005
[11]  Carre, J.E., Orban, J.C., Re, L., et al. (2010) Survival in Critical Ill-ness Is Associated with Early Activation of Mitochondrial Biogenesis. American Journal of Respiratory and Critical Care Medicine, 182, 745-751.
https://doi.org/10.1164/rccm.201003-0326OC
[12]  Gründler, K., Angstwurm, M., Hilge, R., et al. (2014) Platelet Mitochondrial Membrane Depolarization Reflects Disease Severity in Patients with Sepsis and Correlates with Clinical Outcome. Critical Care, 18, Article No. R31.
https://doi.org/10.1186/cc13724
[13]  Japiassu, A.M., Santiago, A.P., D’avila, J.C., et al. (2011) Bioenergetic Fail-ure of Human Peripheral Blood Monocytes in Patients with Septic Shock Is Mediated by Reduced F1Fo Adeno-sine-5’-Triphosphate Synthase Activity. Critical Care Medicine, 39, 1056-1063.
https://doi.org/10.1097/CCM.0b013e31820eda5c
[14]  Suliman, H.B., Welty-Wolf, K.E., Carraway, M., et al. (2004) Lipopolysaccharide Induces Oxidative Cardiac Mitochondrial Damage and Biogenesis. Cardiovascular Research, 64, 279-288.
https://doi.org/10.1016/j.cardiores.2004.07.005
[15]  Smeding, L., Van Der Laarse, W.J., Van Veelen, T.A., et al. (2012) Early Myocardial Dysfunction Is Not Caused by Mitochondrial Abnormalities in a Rat Model of Peritonitis. Journal of Surgical Research, 176, 178-184.
https://doi.org/10.1016/j.jss.2011.05.055
[16]  Correa, T.D., Vuda, M., Blaser, A.R., et al. (2012) Effect of Treat-ment Delay on Disease Severity and Need for Resuscitation in Porcine Fecal Peritonitis. Critical Care Medicine, 40, 2841-2849.
https://doi.org/10.1097/CCM.0b013e31825b916b
[17]  Singer, M., Deutschman, C.S., Seymour, C.W., et al. (2016) The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA, 315, 801-810.
https://doi.org/10.1001/jama.2016.0287
[18]  Uchino, S., Kellum, J.A., Bellomo, R., et al. (2005) Acute Renal Fail-ure in Critically Ill Patients: A Multinational, Multicenter Study. JAMA: Journal of the American Medical Association, 294, 813-818.
https://doi.org/10.1001/jama.294.7.813
[19]  Langenberg, C., Wan, L., Egi, M., et al. (2006) Renal Blood Flow in Experimental Septic Acute Renal Failure. Kidney International, 69, 1996-2002.
https://doi.org/10.1038/sj.ki.5000440
[20]  Houten, S.M., Violante, S., Ventura, F.V. and Wanders, R.J.A. (2016) The Biochemistry and Physiology of Mitochondrial Fatty Acid β-Oxidation and Its Genetic Disorders. Annual Review of Physiology, 78, 23-44.
https://doi.org/10.1146/annurev-physiol-021115-105045
[21]  Wang, Z., Chen, K., Han, Y., et al. (2018) Irisin Protects Heart against Ischemia-Reperfusion Injury through a SOD2-Dependent Mitochondria Mechanism. Journal of Cardiovascular Pharmacology, 72, 259-269.
https://doi.org/10.1097/FJC.0000000000000608
[22]  Ne?i?, L., ?krbi?, R., Amid?i?, L., et al. (2020) Protective Effects of Simvastatin on Endotoxin-Induced Acute Kidney Injury through Activation of Tubular Epithelial Cells’ Sur-vival and Hindering Cytochrome C-Mediated Apoptosis. International Journal of Molecular Sciences, 21, Article 7236.
https://doi.org/10.3390/ijms21197236
[23]  Leduc-Gaudet, J.P., Mayaki, D., Reynaud, O., et al. (2020) Parkin Overexpression Attenuates Sepsis-Induced Muscle Wasting. Cells, 9, Article 1454.
https://doi.org/10.3390/cells9061454
[24]  Tsuji, D., Nakazawa, H., Yorozu, T. and Kaneki, M. (2021) Protective Effects of Farnesyltransferase Inhibitor on Sepsis-Induced Morphological Aberrations of Mitochondria in Muscle and Increased Circulating Mitochondrial DNA Levels in Mice. Biochemical and Biophysical Research Communications, 556, 93-98.
https://doi.org/10.1016/j.bbrc.2021.03.141
[25]  Seymour, C.W., Liu, V.X., Iwashyna, T.J., et al. (2016) Assess-ment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sep-sis-3). JAMA: Journal of the American Medical Association, 315, 762-774.
https://doi.org/10.1001/jama.2016.0288
[26]  Supinski, G.S., Murphy, M.P. and Callahan, L.A. (2009) MitoQ Ad-ministration Prevents Endotoxin-Induced Cardiac Dysfunction. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 297, R1095-R1102.
https://doi.org/10.1152/ajpregu.90902.2008
[27]  Patil, N.K., Parajuli, N., Macmillan-Crow, L.A. and Mayeux, P.R. (2014) Inactivation of Renal Mitochondrial Respiratory Com-plexes and Manganese Superoxide Dismutase during Sepsis: Mitochondria-Targeted Antioxidant Mitigates Injury. American Journal of Physiology-Renal Physiology, 306, F734-F743.
https://doi.org/10.1152/ajprenal.00643.2013
[28]  Powers, S.K., Hudson, M.B., Nelson, W.B., et al. (2011) Mito-chondria-Targeted Antioxidants Protect against Mechanical Ventilation-Induced Diaphragm Weakness. Critical Care Medicine, 39, 1749-1759.
https://doi.org/10.1097/CCM.0b013e3182190b62
[29]  Ganie, S.A., Dar, T.A., Bhat, A.H., et al. (2016) Melatonin: A Potential Anti-Oxidant Therapeutic Agent for Mitochondrial Dysfunctions and Related Disorders. Rejuvenation Re-search, 19, 21-40.
https://doi.org/10.1089/rej.2015.1704
[30]  Srinivasan, V., Mohamed, M. and Kato, H. (2012) Melatonin in Bacte-rial and Viral Infections with Focus on Sepsis: A Review. Recent Patents on Endocrine, Metabolic & Immune Drug Discovery, 6, 30-39.
https://doi.org/10.2174/187221412799015317
[31]  Cowan, D.B., Yao, R., Thedsanamoorthy, J.K., et al. (2017) Transit and Integration of Extracellular Mitochondria in Human Heart Cells. Scientific Reports, 7, Article No. 17450.
https://doi.org/10.1038/s41598-017-17813-0

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