Inflammaging and fatty acid oxidation in monocytes and macrophages-Immunometabolism-CSCIED科技核心评价数据库-手机版

Inflammaging and fatty acid oxidation in monocytes and macrophages

Inflammaging and fatty acid oxidation in monocytes and macrophages

ES评分 0 浏览量：1021 下载量：0

DOI	10.1097/IN9.0000000000000038
刊名	Immunometabolism IJ
年，卷(期)	2024, 6(1)
作者	Kruglov, Victor; Jang, In Hwa; Camell, Christina D.,
作者单位	[Kruglov, Victor; Jang, In Hwa; Camell, Christina D.] Univ Minnesota, Inst Biol Aging & Metab, Dept Biochem Mol Biol & Biophys, Minneapolis, MN 55455 USA
摘要	Fatty acid oxidation (FAO), primarily known as beta-oxidation, plays a crucial role in breaking down fatty acids within mitochondria and peroxisomes to produce cellular energy and preventing metabolic dysfunction. Myeloid cells, including macrophages, microglia, and monocytes, rely on FAO to perform essential cellular functions and uphold tissue homeostasis. As individuals age, these cells show signs of inflammaging, a condition that includes a chronic onset of low-grade inflammation and a decline in metabolic function. These lead to changes in fatty acid metabolism and a decline in FAO pathways. Recent studies have shed light on metabolic shifts occurring in macrophages and monocytes during aging, correlating with an altered tissue environment and the onset of inflammaging. This review aims to provide insights into the connection of inflammatory pathways and altered FAO in macrophages and monocytes from older organisms. We describe a model in which there is an extended activation of receptor for advanced glycation end products, nuclear factor-kappa B (NF-kappa B) and the nod-like receptor family pyrin domain containing 3 inflammasome within macrophages and monocytes. This leads to an increased level of glycolysis, and also promotes pro-inflammatory cytokine production and signaling. As a result, FAO-related enzymes such as 5 ' AMP-activated protein kinase and peroxisome proliferator-activated receptor-alpha are reduced, adding to the escalation of inflammation, accumulation of lipids, and heightened cellular stress. We examine the existing body of literature focused on changes in FAO signaling within macrophages and monocytes and their contribution to the process of inflammaging.
Abstract	Fatty acid oxidation (FAO), primarily known as beta-oxidation, plays a crucial role in breaking down fatty acids within mitochondria and peroxisomes to produce cellular energy and preventing metabolic dysfunction. Myeloid cells, including macrophages, microglia, and monocytes, rely on FAO to perform essential cellular functions and uphold tissue homeostasis. As individuals age, these cells show signs of inflammaging, a condition that includes a chronic onset of low-grade inflammation and a decline in metabolic function. These lead to changes in fatty acid metabolism and a decline in FAO pathways. Recent studies have shed light on metabolic shifts occurring in macrophages and monocytes during aging, correlating with an altered tissue environment and the onset of inflammaging. This review aims to provide insights into the connection of inflammatory pathways and altered FAO in macrophages and monocytes from older organisms. We describe a model in which there is an extended activation of receptor for advanced glycation end products, nuclear factor-kappa B (NF-kappa B) and the nod-like receptor family pyrin domain containing 3 inflammasome within macrophages and monocytes. This leads to an increased level of glycolysis, and also promotes pro-inflammatory cytokine production and signaling. As a result, FAO-related enzymes such as 5 ' AMP-activated protein kinase and peroxisome proliferator-activated receptor-alpha are reduced, adding to the escalation of inflammation, accumulation of lipids, and heightened cellular stress. We examine the existing body of literature focused on changes in FAO signaling within macrophages and monocytes and their contribution to the process of inflammaging.
关键词	aging; cytokines; fatty acid oxidation; inflammaging; inflammasome; inflammation; lipid droplets; macrophages; metabolic disease; microglia; monocytes
KeyWord	aging; cytokines; fatty acid oxidation; inflammaging; inflammasome; inflammation; lipid droplets; macrophages; metabolic disease; microglia; monocytes
基金项目
页码	1-10

参考文献
相关文献

[1]. Franceschi C, Garagnani P, Parini P, et al. Inflammaging: a new immune-metabolic viewpoint for age-related diseases. Nat Rev Endocrinol. 2018;14(10):576-90. doi: 10.1038/s41574-018-0059-4.

[2]. Lee K, Robbins PD, Camell CD. Intersection of immunometabolism and immunosenescence during aging. Curr Opin Pharmacol. 2021;57:107-16. doi: 10.1016/j.coph.2021.01.003.

[3]. Baechle JJ, Chen N, Makhijani P, et al. Chronic inflammation and the hallmarks of aging. Mol Metab. 2023;74:101755. doi: 10.1016/j.molmet.2023.101755.

[4]. Wynn TA, Vannella KM. Macrophages in tissue repair, regeneration, and fibrosis. Immunity. 2016;44(3):450-62. doi: 10.1016/j.immuni.2016.02.015.

[5]. Shi H, Kokoeva MV, Inouye K, et al. TLR4 links innate immunity and fatty acid-induced insulin resistance. J Clin Invest. 2006;116(11):3015-25. doi: 10.1172/JCI28898.

[6]. Murray PJ, Allen JE, Biswas SK, et al. Macrophage activation and polarization: nomenclature and experimental guidelines. Immunity. 2014;41(1):14-20. doi: 10.1016/j.immuni.2014.06.008.

[7]. Yan J, Horng T. Lipid metabolism in regulation of macrophage functions. Trends Cell Biol. 2020;30(12):979-89. doi: 10.1016/j.tcb.2020.09.006.

[8]. Wculek SK, Dunphy G, Heras-Murillo I, et al. Metabolism of tissue macrophages in homeostasis and pathology. Cell Mol Immunol. 2022;19(3):384-408. doi: 10.1038/s41423-021-00791-9.

[9]. Ginhoux F, Guilliams M. Tissue-resident macrophage ontogeny and homeostasis. Immunity. 2016;44(3):439-49. doi: 10.1016/j.immuni.2016.02.024.

[10]. Ortega Martinez de Victoria E, Xu X, Koska J, et al. Macrophage content in subcutaneous adipose tissue: associations with adiposity, age, inflammatory markers, and whole-body insulin action in healthy Pima Indians. Diabetes. 2009;58(2):385-93. doi: 10.2337/db08-0536.

[11]. Trim WV, Walhin JP, Koumanov F, et al. Divergent immunometabolic changes in adipose tissue and skeletal muscle with ageing in healthy humans. J Physiol. 2022;600(4):921-47. doi: 10.1113/JP280977.

[12]. Yu Q, Xiao H, Jedrychowski MP, et al. Sample multiplexing for targeted pathway proteomics in aging mice. Proc Natl Acad Sci U S A. 2020;117(18):9723-32. doi: 10.1073/pnas.1919410117.

[13]. Schaum N, Lehallier B, Hahn O, et al.; Tabula Muris Consortium. Ageing hallmarks exhibit organ-specific temporal signatures. Nature. 2020;583(7817):596-602. doi: 10.1038/s41586-020-2499-y.

[14]. Ou MY, Zhang H, Tan PC, et al. Adipose tissue aging: mechanisms and therapeutic implications. Cell Death Dis. 2022;13(4):300. doi: 10.1038/s41419-022-04752-6.

[15]. Tchernof A, Després JP. Pathophysiology of human visceral obesity: an update. Physiol Rev. 2013;93(1):359-404. doi: 10.1152/physrev.00033.2011.

[16]. Lesnefsky EJ, Chen Q, Hoppel CL. Mitochondrial metabolism in aging heart. Circ Res. 2016;118(10):1593-611. doi: 10.1161/CIRCRESAHA.116.307505.

[17]. Morio B, Hocquette JF, Montaurier C, et al. Muscle fatty acid oxidative capacity is a determinant of whole body fat oxidation in elderly people. Am J Physiol Endocrinol Metab. 2001;280(1):E143-9. doi: 10.1152/ajpendo.2001.280.1.E143.

[18]. Song R, Hu M, Qin X, et al. The roles of lipid metabolism in the pathogenesis of chronic diseases in the elderly. Nutrients. 2023;15(15):3433. doi: 10.3390/nu15153433.

[19]. Chung KW, Lee EK, Lee MK, et al. Impairment of PPARα and the fatty acid oxidation pathway aggravates renal fibrosis during aging. J Am Soc Nephrol. 2018;29(4):1223-37. doi: 10.1681/ASN.2017070802.

[20]. Marschallinger J, Iram T, Zardeneta M, et al. Lipid-droplet-accumulating microglia represent a dysfunctional and proinflammatory state in the aging brain. Nat Neurosci. 2020;23(2):194-208. doi: 10.1038/s41593-019-0566-1.

[21]. Bochkis IM, Przybylski D, Chen J, et al. Changes in nucleosome occupancy associated with metabolic alterations in aged mammalian liver. Cell Rep. 2014;9(3):996-1006. doi: 10.1016/j.celrep.2014.09.048.

[22]. Wang M, Yan Y, Zhang Z, et al. Programmed PPAR-α downregulation induces inflammaging by suppressing fatty acid catabolism in monocytes. iScience. 2021;24(7):102766. doi: 10.1016/j.isci.2021.102766.

[23]. Chung KW, Lee EK, Kim DH, et al. Age-related sensitivity to endotoxin-induced liver inflammation: implication of inflammasome/ , -1β for steatohepatitis. Aging Cell. 2015;14(4):524-33. doi: 10.1111/acel.12305.

[24]. Wan J, Wu X, Chen H, et al. Aging-induced aberrant RAGE/PPARα axis promotes hepatic steatosis via dysfunctional mitochondrial β oxidation. Aging Cell. 2020;19(10). doi: 10.1111/acel.13238.

[25]. Luo R, Su LY, Li G, et al. Activation of PPARA-mediated autophagy reduces Alzheimer disease-like pathology and cognitive decline in a murine model. Autophagy. 2020;16(1):52-69. doi: 10.1080/15548627.2019.1596488.

[26]. Burns JC, Cotleur B, Walther DM, et al. Differential accumulation of storage bodies with aging defines discrete subsets of microglia in the healthy brain. eLife. 2020;9:e57495. doi: 10.7554/eLife.57495.

[27]. Minhas PS, Latif-Hernandez A, McReynolds MR, et al. Restoring metabolism of myeloid cells reverses cognitive decline in ageing. Nature. 2021;590(7844):122-8. doi: 10.1038/s41586-020-03160-0.

[28]. Arbaizar-Rovirosa M, Pedragosa J, Lozano JJ, et al. Aged lipid-laden microglia display impaired responses to stroke. EMBO Mol Med. 2023;15(2):e17175. doi: 10.15252/emmm.202217175.

[29]. Gong H, Chen H, Xiao P, et al. miR-146a impedes the anti-aging effect of AMPK via NAMPT suppression and NAD,/SIRT inactivation. Signal Transduct Target Ther. 2022;7(1):66. doi: 10.1038/s41392-022-00886-3.

[30]. Fang L, Ohashi K, Hayakawa S, et al. Adipolin protects against renal injury via PPARα-dependent reduction of inflammasome activation. iScience. 2023;26(5):106591. doi: 10.1016/j.isci.2023.106591.

[31]. Li Y, Zhu Y, Feng S, et al. Macrophages activated by hepatitis B virus have distinct metabolic profiles and suppress the virus via IL-1β to downregulate PPARα and FOXO3. Cell Rep. 2022;38(4):110284. doi: 10.1016/j.celrep.2021.110284.

[32]. Fang X, Zou S, Zhao Y, et al. Kupffer cells suppress perfluorononanoic acid-induced hepatic peroxisome proliferator-activated receptor α expression by releasing cytokines. Arch Toxicol. 2012;86(10):1515-25. doi: 10.1007/s00204-012-0877-4.

[33]. Mihaylova MM, Cheng CW, Cao AQ, et al. Fasting activates fatty acid oxidation to enhance intestinal stem cell function during homeostasis and aging. Cell Stem Cell. 2018;22(5):769-778.e4. doi: 10.1016/j.stem.2018.04.001.

[34]. Russell DG, Huang L, VanderVen BC. Immunometabolism at the interface between macrophages and pathogens. Nat Rev Immunol. 2019;19(5):291-304. doi: 10.1038/s41577-019-0124-9.

[35]. Liu X, Liu J, Zhao S, et al. Interleukin-4 is essential for Microglia/Macrophage M2 polarization and long-term recovery after cerebral ischemia. Stroke. 2016;47(2):498-504. doi: 10.1161/STROKEAHA.115.012079.

[36]. Sica A, Mantovani A. Macrophage plasticity and polarization: in vivo veritas. J Clin Invest. 2012;122(3):787-95. doi: 10.1172/JCI59643.

[37]. Xie M, Yu Y, Kang R, et al. PKM2-dependent glycolysis promotes NLRP3 and AIM2 inflammasome activation. Nat Commun. 2016;7(1):13280. doi: 10.1038/ncomms13280.

[38]. Lin HC, Chen YJ, Wei YH, et al. Lactic acid fermentation is required for NLRP3 inflammasome activation. Front Immunol. 2021;12:630380. doi: 10.3389/fimmu.2021.630380.

[39]. Duan JX, Jiang HL, Guan XX, et al. Extracellular citrate serves as a DAMP to activate macrophages and promote LPS-induced lung injury in mice. Int Immunopharmacol. 2021;101:108372. doi: 10.1016/j.intimp.2021.108372.

[40]. Palmieri EM, Gonzalez-Cotto M, Baseler WA, et al. Nitric oxide orchestrates metabolic rewiring in M1 macrophages by targeting aconitase 2 and pyruvate dehydrogenase. Nat Commun. 2020;11(1):698. doi: 10.1038/s41467-020-14433-7.

[41]. Li Y, Du Y, Xu Z, et al. Intravital lipid droplet labeling and imaging reveals the phenotypes and functions of individual macrophages in vivo. J Lipid Res. 2022;63(5):100207. doi: 10.1016/j.jlr.2022.100207.

[42]. Rosas-Ballina M, Guan XL, Schmidt A, et al. Classical activation of macrophages leads to lipid droplet formation without de novo fatty acid synthesis. Front Immunol. 2020;11:131. doi: 10.3389/fimmu.2020.00131.

[43]. Viola A, Munari F, Sánchez-Rodríguez R, et al. The metabolic signature of macrophage responses. Front Immunol. 2019;10:1462. doi: 10.3389/fimmu.2019.01462.

[44]. Huang SCC, Everts B, Ivanova Y, et al. Cell-intrinsic lysosomal lipolysis is essential for alternative activation of macrophages. Nat Immunol. 2014;15(9):846-55. doi: 10.1038/ni.2956.

[45]. Tan Z, Xie N, Cui H, et al. Pyruvate dehydrogenase kinase 1 participates in macrophage polarization via regulating glucose metabolism. J Immunol. 2015;194(12):6082-9. doi: 10.4049/jimmunol.1402469.

[46]. Namgaladze D, Brüne B. Fatty acid oxidation is dispensable for human macrophage IL-4-induced polarization. Biochim Biophys Acta. 2014;1841(9):1329-35. doi: 10.1016/j.bbalip.2014.06.007.

[47]. Van den Bossche J, Baardman J, Otto NA, et al. Mitochondrial dysfunction prevents repolarization of inflammatory macrophages. Cell Rep. 2016;17(3):684-96. doi: 10.1016/j.celrep.2016.09.008.

[48]. Divakaruni AS, Hsieh WY, Minarrieta L, et al. Etomoxir inhibits macrophage polarization by disrupting CoA homeostasis. Cell Metab. 2018;28(3):490-503.e7. doi: 10.1016/j.cmet.2018.06.001.

[49]. Nomura M, Liu J, Rovira II, et al. Fatty acid oxidation in macrophage polarization. Nat Immunol. 2016;17(3):216-7. doi: 10.1038/ni.3366.

[50]. Weiss JM, Palmieri EM, Gonzalez-Cotto M, et al. Itaconic acid underpins hepatocyte lipid metabolism in non-alcoholic fatty liver disease in male mice. Nat Metab. 2023;5(6):981-95. doi: 10.1038/s42255-023-00801-2.

[51]. Mills EL, Ryan DG, Prag HA, et al. Itaconate is an anti-inflammatory metabolite that activates Nrf2 via alkylation of KEAP1. Nature. 2018;556(7699):113-7. doi: 10.1038/nature25986.

[52]. Lampropoulou V, Sergushichev A, Bambouskova M, et al. Itaconate links inhibition of succinate dehydrogenase with macrophage metabolic remodeling and regulation of inflammation. Cell Metab. 2016;24(1):158-66. doi: 10.1016/j.cmet.2016.06.004.

[53]. Runtsch MC, Angiari S, Hooftman A, et al. Itaconate and itaconate derivatives target JAK1 to suppress alternative activation of macrophages. Cell Metab. 2022;34(3):487-501.e8. doi: 10.1016/j.cmet.2022.02.002.

[54]. Yao J, Wu D, Qiu Y. Adipose tissue macrophage in obesity-associated metabolic diseases. Front Immunol. 2022;13:977485. doi: 10.3389/fimmu.2022.977485.

[55]. Geng J, Zhang X, Prabhu S, et al. 3D microscopy and deep learning reveal the heterogeneity of crown-like structure microenvironments in intact adipose tissue. Sci Adv. 2021;7(8):eabe2480. doi: 10.1126/sciadv.abe2480.

[56]. Gericke M, Weyer U, Braune J, et al. A method for long-term live imaging of tissue macrophages in adipose tissue explants. Am J Physiol Endocrinol Metab. 2015;308(11):E1023-33. doi: 10.1152/ajpendo.00075.2015.

[57]. Wculek SK, Heras-Murillo I, Mastrangelo A, et al. Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis. Immunity. 2023;56(3):516-30.e9. doi: 10.1016/j.immuni.2023.01.011.

[58]. Dennis EA, Deems RA, Harkewicz R, et al. A mouse macrophage lipidome. J Biol Chem. 2010;285(51):39976-85. doi: 10.1074/jbc.M110.182915.

[59]. Morgan PK, Huynh K, Pernes G, et al. Macrophage polarization state affects lipid composition and the channeling of exogenous fatty acids into endogenous lipid pools. J Biol Chem. 2021;297(6):101341. doi: 10.1016/j.jbc.2021.101341.

[60]. Prieur X, Mok CYL, Velagapudi VR, et al. Differential lipid partitioning between adipocytes and tissue macrophages modulates macrophage lipotoxicity and M2/M1 polarization in obese mice. Diabetes. 2011;60(3):797-809. doi: 10.2337/db10-0705.

[61]. Koliwad SK, Streeper RS, Monetti M, et al. DGAT1-dependent triacylglycerol storage by macrophages protects mice from diet-induced insulin resistance and inflammation. J Clin Invest. 2010;120(3):756-67. doi: 10.1172/JCI36066.

[62]. Dai L, Bhargava P, Stanya KJ, et al. Macrophage alternative activation confers protection against lipotoxicity-induced cell death. Mol Metab. 2017;6(10):1186-97. doi: 10.1016/j.molmet.2017.08.001.

[63]. Sharma BR, Kanneganti TD. NLRP3 inflammasome in cancer and metabolic diseases. Nat Immunol. 2021;22(5):550-9. doi: 10.1038/s41590-021-00886-5.

[64]. Zheng D, Liwinski T, Elinav E. Inflammasome activation and regulation: toward a better understanding of complex mechanisms. Cell Discov. 2020;6:36. doi: 10.1038/s41421-020-0167-x.

[65]. Kim KA, Jeong JJ, Yoo SY, et al. Gut microbiota lipopolysaccharide accelerates inflamm-aging in mice. BMC Microbiol. 2016;16(1):9. doi: 10.1186/s12866-016-0625-7.

[66]. Roh JS, Sohn DH. Damage-associated molecular patterns in inflammatory diseases. Immune Netw. 2018;18(4):e27. doi: 10.4110/in.2018.18.e27.

[67]. Bissonnette S, Lamantia V, Ouimet B, et al. Native low-density lipoproteins are priming signals of the NLRP3 inflammasome/interleukin-1β pathway in human adipose tissue and macrophages. Sci Rep. 2023;13(1):18848. doi: 10.1038/s41598-023-45870-1.

[68]. Ferrucci L, Fabbri E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty. Nat Rev Cardiol. 2018;15(9):505-22. doi: 10.1038/s41569-018-0064-2.

[69]. Becker L, Nguyen L, Gill J, et al. Age-dependent shift in macrophage polarisation causes inflammation-mediated degeneration of enteric nervous system. Gut. 2018;67(5):827-36. doi: 10.1136/gutjnl-2016-312940.

[70]. Liu R, Cui J, Sun Y, et al. Autophagy deficiency promotes M1 macrophage polarization to exacerbate acute liver injury via ATG5 repression during aging. Cell Death Discov. 2021;7(1):397. doi: 10.1038/s41420-021-00797-2.

[71]. Yarbro JR, Emmons RS, Pence BD. Macrophage immunometabolism and inflammaging: roles of mitochondrial dysfunction, cellular senescence, CD38, and NAD. Immunometabolism. 2020;2(3):e200026. doi: 10.20900/immunometab20200026.

[72]. Furman D, Chang J, Lartigue L, et al. Expression of specific inflammasome gene modules stratifies older individuals into two extreme clinical and immunological states. Nat Med. 2017;23(2):174-84. doi: 10.1038/nm.4267.

[73]. Olona A, Leishman S, Anand PK. The NLRP3 inflammasome: regulation by metabolic signals. Trends Immunol. 2022;43(12):978-89. doi: 10.1016/j.it.2022.10.003.

[74]. Ruiz-García A, Monsalve E, Novellasdemunt L, et al. Cooperation of adenosine with macrophage Toll-4 receptor agonists leads to increased glycolytic flux through the enhanced expression of , gene. J Biol Chem. 2011;286(22):19247-58. doi: 10.1074/jbc.M110.190298.

[75]. Finucane OM, Sugrue J, Rubio-Araiz A, et al. The NLRP3 inflammasome modulates glycolysis by increasing PFKFB3 in an IL-1β-dependent manner in macrophages. Sci Rep. 2019;9(1):4034. doi: 10.1038/s41598-019-40619-1.

[76]. Mela V, Mota BC, Milner M, et al. Exercise-induced re-programming of age-related metabolic changes in microglia is accompanied by a reduction in senescent cells. Brain Behav Immun. 2020;87:413-28. doi: 10.1016/j.bbi.2020.01.012.

[77]. Shchukina I, Bagaitkar J, Shpynov O, et al. Enhanced epigenetic profiling of classical human monocytes reveals a specific signature of healthy aging in the DNA methylome. Nat Aging. 2021;1(1):124-41. doi: 10.1038/s43587-020-00002-6.

[78]. Mullican SE, Gaddis CA, Alenghat T, et al. Histone deacetylase 3 is an epigenomic brake in macrophage alternative activation. Genes Dev. 2011;25(23):2480-8. doi: 10.1101/gad.175950.111.

[79]. Chi Z, Chen S, Xu T, et al. Histone deacetylase 3 couples mitochondria to drive IL-1β-dependent inflammation by configuring fatty acid oxidation. Mol Cell. 2020;80(1):43-58.e7. doi: 10.1016/j.molcel.2020.08.015.

[80]. Ghiboub M, Zhao J, Li Yim AYF, et al. HDAC3 mediates the inflammatory response and LPS tolerance in human monocytes and macrophages. Front Immunol. 2020;11:550769. doi: 10.3389/fimmu.2020.550769.

[81]. Dávalos-Salas M, Montgomery MK, Reehorst CM, et al. Deletion of intestinal Hdac3 remodels the lipidome of enterocytes and protects mice from diet-induced obesity. Nat Commun. 2019;10(1):5291. doi: 10.1038/s41467-019-13180-8.

[82]. Ferrari A, Fiorino E, Longo R, et al. Attenuation of diet-induced obesity and induction of white fat browning with a chemical inhibitor of histone deacetylases. Int J Obes (Lond). 2017;41(2):289-98. doi: 10.1038/ijo.2016.191.

[83]. Ferrari A, Longo R, Fiorino E, et al. HDAC3 is a molecular brake of the metabolic switch supporting white adipose tissue browning. Nat Commun. 2017;8(1):93. doi: 10.1038/s41467-017-00182-7.

[84]. Moon JS, Nakahira K, Chung KP, et al. NOX4-dependent fatty acid oxidation promotes NLRP3 inflammasome activation in macrophages. Nat Med. 2016;22(9):1002-12. doi: 10.1038/nm.4153.

[85]. Helfinger V, Palfi K, Weigert A, et al. The NADPH oxidase Nox4 controls macrophage polarization in an NFκB-dependent manner. Oxid Med Cell Longev. 2019;2019:3264858. doi: 10.1155/2019/3264858.

[86]. Mongue-Din H, Patel AS, Looi YH, et al. NADPH Oxidase-4 driven cardiac macrophage polarization protects against myocardial infarction-induced remodeling. JACC Basic Transl Sci. 2017;2(6):688-98. doi: 10.1016/j.jacbts.2017.06.006.

[87]. Camell CD, Sander J, Spadaro O, et al. Inflammasome-driven catecholamine catabolism in macrophages blunts lipolysis during ageing. Nature. 2017;550(7674):119-23. doi: 10.1038/nature24022.

[88]. Petkevicius K, Bidault G, Virtue S, et al. Norepinephrine promotes triglyceride storage in macrophages via beta2-adrenergic receptor activation. FASEB J. 2021;35(2):e21266. doi: 10.1096/fj.202001101R.

[89]. van Dierendonck XAMH, Vrieling F, Smeehuijzen L, et al. Triglyceride breakdown from lipid droplets regulates the inflammatory response in macrophages. Proc Natl Acad Sci U S A. 2022;119(12):e2114739119. doi: 10.1073/pnas.2114739119.

[90]. Zu L, He J, Jiang H, et al. Bacterial endotoxin stimulates adipose lipolysis via toll-like receptor 4 and extracellular signal-regulated kinase pathway. J Biol Chem. 2009;284(9):5915-26. doi: 10.1074/jbc.M807852200.

[91]. van Dierendonck XAMH, de la Rosa Rodriguez MA, Georgiadi A, et al. HILPDA uncouples lipid droplet accumulation in adipose tissue macrophages from inflammation and metabolic dysregulation. Cell Rep. 2020;30(6):1811-1822.e6. doi: 10.1016/j.celrep.2020.01.046.

[92]. Oishi Y, Manabe I. Macrophages in age-related chronic inflammatory diseases. npj Aging Mech Dis. 2016;2(1):16018. doi: 10.1038/npjamd.2016.18.

[93]. De Maeyer RPH, Chambers ES. The impact of ageing on monocytes and macrophages. Immunol Lett. 2021;230:1-10. doi: 10.1016/j.imlet.2020.12.003.

[94]. Leone TC, Weinheimer CJ, Kelly DP. A critical role for the peroxisome proliferator-activated receptor α (PPARα) in the cellular fasting response: the PPARα-null mouse as a model of fatty acid oxidation disorders. Proc Natl Acad Sci USA. 1999;96(13):7473-8. doi: 10.1073/pnas.96.13.7473.

[95]. Kilu W, Merk D, Steinhilber D, et al. Heterodimer formation with retinoic acid receptor RXRα modulates coactivator recruitment by peroxisome proliferator-activated receptor PPARγ. J Biol Chem. 2021;297(1):100814. doi: 10.1016/j.jbc.2021.100814.

[96]. Twarda-Clapa A, Olczak A, Białkowska AM, et al. Advanced Glycation End-Products (AGEs): formation, chemistry, classification, receptors, and diseases related to AGEs. Cells. 2022;11(8):1312. doi: 10.3390/cells11081312.

[97]. Byun K, Yoo Y, Son M, et al. Advanced glycation end-products produced systemically and by macrophages: a common contributor to inflammation and degenerative diseases. Pharmacol Ther. 2017;177:44-55. doi: 10.1016/j.pharmthera.2017.02.030.

[98]. Talma N, Gerrits E, Wang B, et al. Identification of distinct and age-dependent p16 , microglia subtypes. Aging Cell. 2021;20(10):13450. doi: 10.1111/acel.13450.

[99]. Salminen A, Kaarniranta K. AMP-activated protein kinase (AMPK) controls the aging process via an integrated signaling network. Ageing Res Rev. 2012;11(2):230-41. doi: 10.1016/j.arr.2011.12.005.

[100]. Sag D, Carling D, Stout RD, et al. Adenosine 5′-Monophosphate-Activated protein kinase promotes macrophage polarization to an anti-inflammatory functional phenotype. J Immunol. 2008;181(12):8633-41. doi: 10.4049/jimmunol.181.12.8633.

[101]. Galic S, Fullerton MD, Schertzer JD, et al. Hematopoietic AMPK β1 reduces mouse adipose tissue macrophage inflammation and insulin resistance in obesity. J Clin Invest. 2011;121(12):4903-15. doi: 10.1172/JCI58577.

[102]. Steinberg GR, Schertzer JD. AMPK promotes macrophage fatty acid oxidative metabolism to mitigate inflammation: implications for diabetes and cardiovascular disease. Immunol Cell Biol. 2014;92(4):340-5. doi: 10.1038/icb.2014.11.

[103]. Zhang M, Zhu H, Ding Y, et al. AMP-activated protein kinase α1 promotes atherogenesis by increasing monocyte-to-macrophage differentiation. J Biol Chem. 2017;292(19):7888-903. doi: 10.1074/jbc.M117.779447.

[104]. Zhu Y, Dun H, Ye L, et al. Targeting fatty acid β-oxidation impairs monocyte differentiation and prolongs heart allograft survival. JCI Insight. 2022;7(7):e151596. doi: 10.1172/jci.insight.151596.

[105]. Raulien N, Friedrich K, Strobel S, et al. Fatty acid oxidation compensates for lipopolysaccharide-induced warburg effect in glucose-deprived monocytes. Front Immunol. 2017;8:609. doi: 10.3389/fimmu.2017.00609.

[106]. Funahashi K, Cao X, Yamauchi M, et al. Prostaglandin E2 negatively regulates AMP-activated protein kinase via protein kinase a signaling pathway. Prostaglandins Other Lipid Mediat. 2009;88(1-2):31-5. doi: 10.1016/j.prostaglandins.2008.09.002.

[107]. Cantó C, Gerhart-Hines Z, Feige JN, et al. AMPK regulates energy expenditure by modulating NAD, metabolism and SIRT1 activity. Nature. 2009;458(7241):1056-60. doi: 10.1038/nature07813.

[108]. Jung ES, Suh K, Han J, et al. Amyloid-β activates NLRP3 inflammasomes by affecting microglial immunometabolism through the Syk-AMPK pathway. Aging Cell. 2022;21(5):e13623. doi: 10.1111/acel.13623.

[109]. Yang Z, Kahn BB, Shi H, et al. Macrophage α1 AMP-activated protein kinase (α1AMPK) antagonizes fatty acid-induced inflammation through SIRT1. J Biol Chem. 2010;285(25):19051-9. doi: 10.1074/jbc.M110.123620.

[110]. Dobri AM, Dudău M, Enciu AM, et al. CD36 in alzheimer’s disease: an overview of molecular mechanisms and therapeutic targeting. Neuroscience. 2021;453:301-11. doi: 10.1016/j.neuroscience.2020.11.003.

[111]. Grajchen E, Wouters E, Van De Haterd B, et al. CD36-mediated uptake of myelin debris by macrophages and microglia reduces neuroinflammation. J Neuroinflammation. 2020;17(1):224. doi: 10.1186/s12974-020-01899-x.

[112]. Yarbro JR, Pence BD. Classical monocytes from older adults maintain capacity for metabolic compensation during glucose deprivation and lipopolysaccharide stimulation. Mech Ageing Dev. 2019;183:111146. doi: 10.1016/j.mad.2019.111146.

[113]. Anderson RM, Weindruch R. Metabolic reprogramming, caloric restriction and aging. Trends Endocrinol Metab. 2010;21(3):134-41. doi: 10.1016/j.tem.2009.11.005.

[114]. López-Lluch G, Navas P. Calorie restriction as an intervention in ageing: calorie restriction and ageing. J Physiol. 2016;594(8):2043-60. doi: 10.1113/JP270543.

[115]. Mohammed I, Hollenberg MD, Ding H, et al. A critical review of the evidence that metformin is a putative anti-aging drug that enhances healthspan and extends lifespan. Front Endocrinol. 2021;12:718942. doi: 10.3389/fendo.2021.718942.

[116]. Chen S, Gan D, Lin S, et al. Metformin in aging and aging-related diseases: clinical applications and relevant mechanisms. Theranostics. 2022;12(6):2722-40. doi: 10.7150/thno.71360.

[117]. Cuyàs E, Verdura S, Llorach-Parés L, et al. Metformin is a direct SIRT1-Activating compound: computational modeling and experimental validation. Front Endocrinol. 2018;9:657. doi: 10.3389/fendo.2018.00657.

[118]. Martin-Montalvo A, Mercken EM, Mitchell SJ, et al. Metformin improves healthspan and lifespan in mice. Nat Commun. 2013;4(1):2192. doi: 10.1038/ncomms3192.

[119]. Noren Hooten N, Martin-Montalvo A, Dluzen DF, et al. Metformin-mediated increase in DICER1 regulates microRNA expression and cellular senescence. Aging Cell. 2016;15(3):572-81. doi: 10.1111/acel.12469.,

引用本文

Kruglov, Victor; Jang, In Hwa; Camell, Christina D.. Inflammaging and fatty acid oxidation in monocytes and macrophages [J]. Immunometabolism. 2024; 6; (1). 1 - 10.

文献评论

相关学者

相关机构