👤 MP Mattson

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Also published as: M. P. Mattson,
articles
C. Crivelli, S. Garcia-Madrona, M. Gil-Minguez +428 more · 2024 · Frontiers in Neuroscience · Frontiers · added 2026-04-20
C. Crivelli, S. Garcia-Madrona, M. Gil-Minguez, R. Lujan, A. Almeida, S. Moncada, J. P. Bolanos, C. Angebault, J. Fauconnier, S. Patergnani, J. Rieusset, A. Danese, C. A. Affortit, A. Ardalan, S. Sowlati-Hashjin, H. Oduwoye, S. O. Uwumarenogie, M. Karttunen, M. D. Smith, A. Atlante, G. Amadoro, V. Latina, D. Valenti, M. Belanger, I. Allaman, P. J. Magistretti, K. F. Bell, B. Al-Mubarak, J. H. Fowler, P. S. Baxter, K. Gupta, T. Tsujita, A. M. Bertholet, A. M. Natale, P. Bisignano, J. Suzuki, A. Fedorenko, J. Hamilton, C. Bienboire-Frosini, D. Wang, M. Marcet-Rius, D. Villanueva-Garcia, A. Gazzano, A. Dominguez-Oliva, M. Bienengraeber, K. S. Echtay, M. Klingenberg, C. Bionda, J. Portoukalian, D. Schmitt, C. Rodriguez-Lafrasse, D. Ardail, M. Bozluolcay, G. Andican, S. Firtina, G. Erkol, D. Konukoglu, R. D. Burgoyne, D. A. Butterfield, B. Halliwell, M. Cater, S. M. Holter, K. A. Chamberlain, N. Huang, Y. Xie, F. LiCausi, S. Li, Y. Li, S. L. Chan, D. Liu, G. A. Kyriazis, P. Bagsiyao, X. Ouyang, M. P. Mattson, W. Chen, J. Yang, S. Chen, H. Xiang, H. Liu, D. Lin, Z. Chen, C. Zhong, I. Cho, G. J. Hwang, J. H. Cho, H. O. Song, H. E. Ji, S. Yang, A. C. Chu, P. W. Ho, K. H. Kwok, J. W. Ho, K. H. Chan, H. F. Liu, E. H. Corder, A. M. Saunders, W. J. Strittmatter, D. E. Schmechel, P. C. Gaskell, G. W. Small, S. M. Crivelli, Z. Quadri, H. J. Vekaria, Z. Zhu, P. Tripathi, A. Elsherbini, J. Cummings, Y. Zhou, G. Lee, K. Zhong, J. Fonseca, F. Cheng, C. H. Davis, K. Y. Kim, E. A. Bushong, E. A. Mills, D. Boassa, T. Shih, S. M. de la Monte, J. R. Wands, L. E. de Vries, A. Jongejan, J. Monteiro Fortes, R. Balesar, A. J. M. Rozemuller, P. D. Moerland, G. A. Dienel, D. L. Rothman, R. Domingues, C. Pereira, M. T. Cruz, A. Silva, R. Dringen, J. M. Gutterer, J. Hirrlinger, H. H. Hoepken, T. Minich, C. Ruedig, A. Lajtha, G. E. Gibson, R. H. Du, F. F. Wu, M. Lu, X. D. Shu, J. H. Ding, G. Wu, E. Winkler, J. Fortea, J. Pegueroles, D. Alcolea, O. Belbin, O. Dols-Icardo, L. Vaque-Alcazar, P. Garcia-Nogales, K. D. Garlid, M. Jaburek, P. Jezek, D. E. Orosz, M. Modriansky, S. Vassanelli, K. N. Green, H. Khashwji, T. Estrada, F. M. LaFerla, J. Grundlingh, P. I. Dargan, M. El-Zanfaly, D. M. Wood, A. Gustavsson, N. Norton, T. Fast, L. Frolich, J. Georges, D. Holzapfel, J. N. Guzman, J. Sanchez-Padilla, D. Wokosin, J. Kondapalli, E. Ilijic, P. T. Schumacker, A. Habas, J. Hahn, X. Wang, M. Margeta, P. Hanak, K. Hayakawa, E. Esposito, Y. Terasaki, Y. Liu, C. Xing, A. Herrero-Mendez, E. Fernandez, C. Maestre, D. H. So, Z. H. Tse, H. M. Tse, D. C. Yiu, W. Y. Zhang, T. Hoang, M. Kuljanin, M. Jelokhani-Niaraki, K. A. Hogan, C. C. S. Chini, E. N. Chini, N. Hu, Y. Fu, W. F. Li, X. R. Yang, M. Cao, F. F. Li, S. G. Huang, M. O. Isei, M. Crockett, E. Chen, J. Rodwell-Bullock, T. Caroll, P. A. Girardi, M. V. Ivanova, F. R. McSorley, G. Krnac, H. T. Jacobs, D. Jiang, H. Lu, D. Jimenez-Blasco, P. Santofimia-Castano, A. Gonzalez, Y. Jing, Y. Niu, C. Liu, K. Zen, D. Li, J. M. Johnson, A. D. Peterlin, E. Balderas, E. G. Sustarsic, J. A. Maschek, M. J. Lang, S. M. Joksimovic, P. Eggan, Y. Izumi, S. L. Joksimovic, V. Tesic, R. M. Dietz, S. M. Ghodsi, J. A. Heinsbroek, J. E. Orfila, N. Busquet, B. Kaltschmidt, M. Uherek, B. Volk, P. A. Baeuerle, C. Kaltschmidt, Y. Kang, L. Chen, D. Kapogiannis, K. I. Avgerinos, B. M. Kenwood, J. L. Weaver, A. Bajwa, I. K. Poon, F. L. Byrne, B. A. Murrow, E. Klotzsch, A. Smorodchenko, L. Lofler, R. Moldzio, E. Parkinson, G. J. Schutz, N. Kyrtata, H. C. A. Emsley, O. Sparasci, L. M. Parkes, B. R. Dickie, Y. Lee, B. M. Morrison, S. Lengacher, M. H. Farah, P. N. Hoffman, S. A. Liddelow, K. A. Guttenplan, L. E. Clarke, F. C. Bennett, C. J. Bohlen, L. Schirmer, N. C. de Souza-Pinto, J. R. Slevin, R. P. Wersto, M. Zhan, J. Y. Chatton, M. Manczak, M. J. Calkins, P. H. Reddy, W. Mao, X. X. Yu, A. Zhong, W. Li, J. Brush, S. W. Sherwood, A. Montesanto, P. Crocco, M. Anfossi, N. Smirne, G. Puccio, R. Colao, S. Moriguchi, N. Shioda, Y. Yamamoto, H. Tagashira, K. Fukunaga, H. Morton, S. Kshirsagar, E. Orlov, L. E. Bunquin, N. Sawant, L. Boleng, L. Mosconi, R. D. Andrews, D. C. Matthews, T. Y. Nakamura, S. Nakao, S. Wakabayashi, K. F. Neumann, L. Rojo, L. P. Navarrete, G. Farias, P. Reyes, R. B. Maccioni, D. G. Nicholls, S. Oddo, A. Caccamo, J. D. Shepherd, M. P. Murphy, T. E. Golde, R. Kayed, D. M. A. Oliver, W. R. Pearson, L. Pellerin, A. K. Bouzier-Sore, A. Aubert, S. Serres, M. Merle, R. Costalat, H. Perreten Lambert, M. Zenger, G. Azarias, R. J. Perry, D. Zhang, X. M. Zhang, J. L. Boyer, G. I. Shulman, C. Petersen, M. D. Nielsen, E. S. Andersen, A. L. Basse, M. S. Isidor, L. K. Markussen, T. Philips, J. D. Rothstein, C. Poetschke, J. Duda, J. Benkert, E. Dragicevic, T. P. Snutch, J. Striessnig, J. A. Pradeepkiran, R. A. Rice, N. C. Berchtold, C. W. Cotman, N. Rosenberg, M. Reva, F. Binda, L. Restivo, P. Depierre, J. Puyal, J. J. Ruprecht, E. R. S. Kunji, A. S. Saab, I. D. Tzvetanova, K. A. Nave, I. D. Tzvetavona, A. Trevisiol, S. Baltan, P. Dibaj, K. Kusch, A. Serrano-Pozo, Z. Li, A. Noori, H. N. Nguyen, A. Mezlini, L. Li, M. Sheridan, B. Ogretmen, C. Simons, N. Deuter, O. Pongs, T. Schneider, A. Rupprecht, I. Sarilova, O. Ninnemann, A. U. Brauer, K. Franke, G. E. Stutzmann, I. Smith, I. Parker, R. H. Swerdlow, R. Thangavel, D. Kempuraj, S. Zaheer, S. Raikwar, M. E. Ahmed, G. P. Selvakumar, B. Vaccari-Cardoso, M. Antipina, A. G. Teschemacher, S. Kasparov, B. R. Villa, A. G. George, T. E. Shutt, P. G. Sullivan, J. M. Rho, G. C. Teskey, A. A. Willette, B. B. Bendlin, E. J. Starks, A. C. Birdsill, S. C. Johnson, B. T. Christian, S. Q. Xu, X. D. Yang, Y. W. Qian, Q. Xiao Show less
The brain’s high demand for energy necessitates tightly regulated metabolic pathways to sustain physiological activity. Glucose, the primary energy substrate, undergoes complex metabolic transformatio Show more
The brain’s high demand for energy necessitates tightly regulated metabolic pathways to sustain physiological activity. Glucose, the primary energy substrate, undergoes complex metabolic transformations, with mitochondria playing a central role in ATP production via oxidative phosphorylation. Dysregulation of this metabolic interplay is implicated in Alzheimer’s disease (AD), where compromised glucose metabolism, oxidative stress, and mitochondrial dysfunction contribute to disease progression. This review explores the intricate bioenergetic crosstalk between astrocytes and neurons, highlighting the function of mitochondrial uncoupling proteins (UCPs), particularly UCP4, as important regulators of brain metabolism and neuronal function. Predominantly expressed in the brain, UCP4 reduces the membrane potential in the inner mitochondrial membrane, thereby potentially decreasing the generation of reactive oxygen species. Furthermore, UCP4 mitigates mitochondrial calcium overload and sustains cellular ATP levels through a metabolic shift from mitochondrial respiration to glycolysis. Interestingly, the levels of the neuronal UCPs, UCP2, 4 and 5 are significantly reduced in AD brain tissue and a specific UCP4 variant has been associated to an increased risk of developing AD. Few studies modulating the expression of UCP4 in astrocytes or neurons have highlighted protective effects against neurodegeneration and aging, suggesting that pharmacological strategies aimed at activating UCPs, such as protonophoric uncouplers, hold promise for therapeutic interventions in AD and other neurodegenerative diseases. Despite significant advances, our understanding of UCPs in brain metabolism remains in its early stages, emphasizing the need for further research to unravel their biological functions in the brain and their therapeutic potential. Show less
đź“„ PDF DOI: 10.3389/fnins.2024.1483708
ROS amino-acid mitochondria review
T Marx, J Yang, S Zhou +216 more · 2022 · Cancer & Metabolism · BioMed Central · added 2026-04-20
T Marx, J Yang, S Zhou, Y Wang, Y Li, X Tong, F Guerra, AA Arbini, L Moro, M Huttemann, I Lee, LI Grossman, JW Doan, TH Sanderson, R Diaz-Ruiz, M Rigoulet, A Devin, WH Koppenol, PL Bounds, CV Dang, E Gottlieb, KH Vousden, OD Maddocks, D Hanahan, RA Weinberg, NP Echeverri Ruiz, V Mohan, J Wu, S Scott, M Kreamer, M Benej, T Golias, I Papandreou, NC Denko, MA Desbats, I Giacomini, T Prayer-Galetti, M Montopoli, CS Ahn, CM Metallo, VC Fogg, NJ Lanning, JP Mackeigan, YK Shin, BC Yoo, YS Hong, HJ Chang, KH Jung, SY Jeong, JG Park, MM Schroll, GJ LaBonia, KR Ludwig, AB Hummon, RL Siegel, KD Miller, A Goding Sauer, SA Fedewa, LF Butterly, JC Anderson, A Cercek, RA Smith, A Jemal, S Brandhorst, VD Longo, A Nencioni, I Caffa, S Cortellino, Y Liang, J Liu, Z Feng, CR Berkers, SM Mason, L Zheng, K Blyth, F Yang, SS Teves, CJ Kemp, S Henikoff, K Fujita, Y Kubota, H Ishida, Y Sasaki, A Signes, E Fernandez-Vizarra, Y Chaban, EJ Boekema, NV Dudkina, C Maletzki, S Stier, U Gruenert, M Gock, C Ostwald, F Prall, M Linnebacher, K Prabst, H Engelhardt, S Ringgeler, H Hubner, AV Kudryavtseva, GS Krasnov, AA Dmitriev, BY Alekseev, OL Kardymon, AF Sadritdinova, MS Fedorova, AV Pokrovsky, NV Melnikova, AD Kaprin, M Skrtic, S Sriskanthadevan, B Jhas, M Gebbia, X Wang, Z Wang, R Hurren, Y Jitkova, M Gronda, N Maclean, Y Chen, E McMillan-Ward, J Kong, SJ Israels, SB Gibson, AC Little, I Kovalenko, LE Goo, HS Hong, SA Kerk, JA Yates, V Purohit, DB Lombard, SD Merajver, CA Lyssiotis, C Bailly, SA Huisman, P de Bruijn, IM Ghobadi Moghaddam-Helmantel, CF Labuschagne, NJ van den Broek, GM Mackay, EF Fang, H Kassahun, DL Croteau, M Scheibye-Knudsen, K Marosi, H Lu, RA Shamanna, S Kalyanasundaram, RC Bollineni, MA Wilson, KF Chua, MP Mattson, VA Bohr, MO Turgeon, NJS Perry, G Poulogiannis, Y Rai, R Pathak, N Kumari, DK Sah, S Pandey, N Kalra, R Soni, BS Dwarakanath, AN Bhatt, JE Hutton, LJ Zimmerman, RJ Slebos, IA Trenary, JD Young, M Li, DC Liebler, M Tabuso, M Christian, PK Kimani, K Gopalakrishnan, RP Arasaradnam, BJ Altman, ZE Stine, J Yun, C Rago, I Cheong, R Pagliarini, P Angenendt, H Rajagopalan, K Schmidt, JK Willson, S Markowitz, G Giachin, R Bouverot, S Acajjaoui, S Pantalone, M Soler-Lopez, C Gorrini, IS Harris, TW Mak, S Vogt, A Rhiel, P Weber, R Ramzan, BB Das, A Ghosh, S Bhattacharjee, A Bhattacharyya, Y Pommier, E Leo, H Zhang, C Marchand, TM Ashton, WG McKenna, LA Kunz-Schughart, GS Higgins, A Bansal, MC Simon, L Marx-Blumel, C Marx, M Kuhne, J Sonnemann Show less
Background Metabolic adaptations can allow cancer cells to survive DNA-damaging chemotherapy. This unmet clinical challenge is a potential vulnerability of cancer. Accordingly, there is an intense se Show more
Background Metabolic adaptations can allow cancer cells to survive DNA-damaging chemotherapy. This unmet clinical challenge is a potential vulnerability of cancer. Accordingly, there is an intense search for mechanisms that modulate cell metabolism during anti-tumor therapy. We set out to define how colorectal cancer CRC cells alter their metabolism upon DNA replication stress and whether this provides opportunities to eliminate such cells more efficiently. Methods We incubated p53-positive and p53-negative permanent CRC cells and short-term cultured primary CRC cells with the topoisomerase-1 inhibitor irinotecan and other drugs that cause DNA replication stress and consequently DNA damage. We analyzed pro-apoptotic mitochondrial membrane depolarization and cell death with flow cytometry. We evaluated cellular metabolism with immunoblotting of electron transport chain (ETC) complex subunits, analysis of mitochondrial mRNA expression by qPCR, MTT assay, measurements of oxygen consumption and reactive oxygen species (ROS), and metabolic flux analysis with the Seahorse platform. Global metabolic alterations were assessed using targeted mass spectrometric analysis of extra- and intracellular metabolites. Results Chemotherapeutics that cause DNA replication stress induce metabolic changes in p53-positive and p53-negative CRC cells. Irinotecan enhances glycolysis, oxygen consumption, mitochondrial ETC activation, and ROS production in CRC cells. This is connected to increased levels of electron transport chain complexes involving mitochondrial translation. Mass spectrometric analysis reveals global metabolic adaptations of CRC cells to irinotecan, including the glycolysis, tricarboxylic acid cycle, and pentose phosphate pathways. P53-proficient CRC cells, however, have a more active metabolism upon DNA replication stress than their p53-deficient counterparts. This metabolic switch is a vulnerability of p53-positive cells to irinotecan-induced apoptosis under glucose-restricted conditions. Conclusion Drugs that cause DNA replication stress increase the metabolism of CRC cells. Glucose restriction might improve the effectiveness of classical chemotherapy against p53-positive CRC cells. Graphical Abstract The topoisomerase-1 inhibitor irinotecan and other chemotherapeutics that cause DNA damage induce metabolic adaptations in colorectal cancer (CRC) cells irrespective of their p53 status. Irinotecan enhances the glycolysis and oxygen consumption in CRC cells to deliver energy and biomolecules necessary for DNA repair and their survival. Compared to p53-deficient cells, p53-proficient CRC cells have a more active metabolism and use their intracellular metabolites more extensively. This metabolic switch creates a vulnerability to chemotherapy under glucose-restricted conditions for p53-positive cells. Supplementary Information The online version contains supplementary material available at 10.1186/s40170-022-00286-9. Show less
đź“„ PDF DOI: 10.1186/s40170-022-00286-9
DNA-binding ROS mitochondria
JP Ježek, AGW Leslie, R Lutter +1993 more · 2018 · Antioxidants & redox signaling · added 2026-04-20
JP Ježek, AGW Leslie, R Lutter, JE Walker, AE Adams, AM Carroll, PG Fallon, RK Porter, O Hanrahan, DN Nolan, HP Voorheis, P Fallon, OM Kelly, C Affourtit, MD Brand, M Jastroch, C Aguer, BD Piccolo, O Fiehn, SH Adams, ME Harper, L Alán, K Smolková, E Kronusová, J Šantorová, P Ježek, EM Allister, CA Robson-Doucette, KJ Prentice, AB Hardy, S Sultan, HY Gaisano, D Kong, P Gilon, PL Herrera, BB Lowell, MB Wheeler, R Amat, G Solanes, M Giralt, F Villarroya, ZB Andrews, ZW Liu, N Walllingford, DM Erion, E Borok, JM Friedman, MH Tschöp, M Shanabrough, G Cline, GI Shulman, A Coppola, XB Gao, TL Horvath, S Diano, MA Aon, S Cortassa, E Marbán, B O'Rourke, H Aquila, TA Link, M Klingenberg, D Arsenijevic, H Onuma, C Pecqueur, S Raimbault, BS Manning, B Miroux, E Couplan, MC Alves-Guerra, M Goubern, R Surwit, F Bouillaud, D Richard, S Collins, D Ricquier, V Ayyasamy, KM Owens, MM Desouki, P Liang, A Bakin, K Thangaraj, DJ Buchsbaum, AF LoBuglio, KK Singh, V Azzu, EP Breen, N Parker, G Baffy, Z Derdak, SC Robson, Y Bai, X Bai, AV Medvedev, M Misukonis, JB Weinberg, W Cao, J Robidoux, LM Floering, KW Daniel, KA Ball, AW Nelson, DG Foster, RO Poyton, J Barlow, V Hirschberg Jensen, CJ Barnstable, R Reddy, H Li, W Basu Ball, S Kar, M Mukherjee, AG Chande, R Mukhopadhyaya, PK Das, JM Baughman, F Perocchi, HS Girgis, M Plovanich, CA Belcher-Timme, Y Sancak, XR Bao, L Strittmatter, O Goldberger, RL Bogorad, V Koteliansky, VK Mootha, V Beck, M Jabůrek, EE Pohl, T Demina, A Rupprecht, EL Bell, TA Klimova, J Eisenbart, CT Moraes, MP Murphy, GRS Budinger, NS Chandel, MJ Berardi, JJ Chou, WM Shih, SC Harrison, M Bertolotti, G Farinelli, M Galli, A Aiuti, R Sitia, J Blanc, B Esposito, S Rousset, P Gourdy, A Tedgui, Z Mallat, L Bleier, S Dröse, M Board, C Lopez, C van den Bos, R Callaghan, K Clarke, C Carr, AI Bondarenko, W Parichatikanond, CT Madreiter, R Rost, M Waldeck-Weiermair, R Malli, WF Graier, J Borecký, D Siemen, O Boss, S Samec, A Paoloni-Giacobino, C Rossier, A Dulloo, J Seydoux, P Muzzin, JP Giacobino, S Boudina, S Sena, BT O'Neill, P Tathireddy, ME Young, ED Abel, H Theobald, X Sheng, JJ Wright, XH Xia, S Aziz, JI Johnson, H Bugger, VG Zaha, TC Esteves, J Brandi, D Cecconi, M Cordani, M Torrens-Mas, R Pacchiana, E Dalla Pozza, G Butera, M Manfredi, E Marengo, J Oliver, P Roca, I Dando, M Donadelli, MO Breckwoldt, FMJ Pfister, PM Bradley, P Marinković, PR Williams, MS Brill, B Plomer, A Schmalz, DK St Clair, R Naumann, O Griesbeck, M Schwarzländer, L Godinho, FM Bareyre, TP Dick, M Kerschensteiner, T Misgeld, W Pilgrim, KJ Clarke, C Yssel, M Farrell, J Zhou, PV Murphy, PS Brookes, JA Buckingham, A Vidal-Puig, AP Halestrap, TE Gunter, DG Nicholls, P Bernardi, JJ Lemasters, A Bugge, M Siersbæk, MS Madsen, A Göndör, C Rougier, S Mandrup, C Guzman, C Zechner, M Palmeri, KS Russell, RR Russell, JA Cabrera, EA Ziemba, R Colbert, RF Kelly, M Kuskowski, EA Arriaga, W Sluiter, DJ Duncker, HB Ward, EO McFalls, V Calegari, CC Zoppi, L Rezende, L Silveira, E Carneiro, AC Boschero, B Cannon, IG Shabalina, TV Kramarova, N Petrovic, J Nedergaard, A Caron, SM Labbé, S Carter, MC Roy, R Lecomte, F Picard, LR Haines, TW Pearson, CM Walsh, CM Brennan, E Casanova, L Baselga-Escudero, A Ribas-Latre, A Arola-Arnal, C Bladé, L Arola, MJ Salvadó, HZ Chae, H Oubrahim, JW Park, SG Rhee, PB Chock, CB Chan, SL Chan, D Liu, GA Kyriazis, P Bagsiyao, X Ouyang, MP Mattson, L Chaudhuri, RK Srivastava, F Kos, PA Shrikant, M Che, R Wang, X Li, HY Wang, XFS Zheng, C Chen, K Wang, J Chen, J Guo, Y Yin, X Cai, X Guo, G Wang, R Yang, L Zhu, Y Zhang, J Wang, Y Xiang, C Weng, K Zen, J Zhang, CY Zhang, Y Chen, J Liu, Y Zheng, Z Wang, S Gu, J Tan, Q Jing, H Yang, J Cheng, G Nanayakkara, Y Shao, R Cueto, L Wang, WY Yang, Y Tian, H Wang, X Yang, N Cheurfa, D Dubois-Laforgue, DAF Ferrarezi, AF Reis, GM Brenner, C Bouche, C Le Feuvre, F Fumeron, J Timsit, M Marre, G Velho, SY Cho, D Seo, WG Kim, S Lee, YS Cho, JH Lee, KH Jung, SH Moon, YS Choe, KH Lee, ET Chouchani, L Kazak, MP Jedrychowski, GZ Lu, BK Erickson, J Szpyt, KA Pierce, D Laznik-Bogoslavski, R Vetrivelan, CB Clish, AJ Robinson, SP Gygi, BM Spiegelman, C Methner, G Buonincontri, CH Hu, A Logan, SJ Sawiak, T Krieg, VR Pell, E Gaude, D Aksentijević, SY Sundier, EL Robb, SM Nadtochiy, ENJ Ord, AC Smith, F Eyassu, R Shirley, C-H Hu, AJ Dare, AM James, S Rogatti, RC Hartley, S Eaton, ASH Costa, SM Davidson, MR Duchen, K Saeb-Parsy, MJ Shattock, LM Work, C Frezza, YC Chuang, TK Lin, HY Huang, WN Chang, CW Liou, SD Chen, AY Chang, SH Chan, L Contreras, E Rial, S Cerdan, J Satrustegui, E Paradis, A Corcoran, TG Cotter, D Cosentino-Gomes, N Rocco-Machado, JR Meyer-Fernandes, LF Costa Rosa, R Curi, C Murphy, P Newsholme, MDM Gonzalez-Barroso, PG Crichton, Y Lee, ERS Kunji, MD Cruz, S Ledbetter, S Chowdhury, AK Tiwari, N Momi, RK Wali, C Bliss, C Huang, D Lichtenstein, S Bhattacharya, A Varma-Wilson, V Backman, HK Roy, M D'Adamo, L Perego, M Cardellini, MA Marini, S Frontoni, F Andreozzi, A Sciacqua, D Lauro, P Sbraccia, M Federici, M Paganelli, AE Pontiroli, R Lauro, F Perticone, F Folli, G Sesti, A Daiber, F Di Lisa, M Oelze, S Kröller-Schön, S Steven, E Schulz, T Münzel, LT Dalgaard, G Andersen, LH Larsen, TIA Sørensen, T Andersen, T Drivsholm, K Borch-Johnsen, J Fleckner, T Hansen, N Din, O Pedersen, C Fiorini, ED Pozza, C Padroni, C Costanzo, M Palmieri, S Dato, F De Rango, P Crocco, G Passarino, G Rose, PBM De Andrade, M Casimir, P Maechler, P De Lange, A Feola, M Ragni, R Senese, M Moreno, A Lombardi, E Silvestri, F Goglia, A Lanni, U De Marchi, C Castelbou, N Demaurex, R De Simone, MA Ajmone-Cat, M Pandolfi, A Bernardo, C De Nuccio, L Minghetti, S Visentin, D De Stefani, A Raffaello, E Teardo, I Szabò, R Rizzuto, T Pozzan, G Den Besten, A Bleeker, A Gerding, K Van Eunen, R Havinga, TH Van Dijk, MH Oosterveer, JW Jonker, AK Groen, DJ Reijngoud, BM Bakker, Z Derdák, P Fülöp, E Sabo, R Tavares, EP Berthiaume, MB Resnick, G Paragh, JR Wands, NM Mark, G Beldi, SS Dhamrait, JW Stephens, JA Cooper, J Acharya, AR Mani, K Moore, GJ Miller, SE Humphries, SJ Hurel, HE Montgomery, JK Jeong, MO Dietrich, HB Ruan, E Kim, S Suyama, K Kelly, E Gyengesi, JL Arbiser, DD Belsham, DA Sarruf, MW Schwartz, AM Bennett, CV Mobbs, WX Ding, M Li, JM Biazik, DG Morgan, F Guo, HM Ni, M Goheen, EL Eskelinen, XM Yin, AS Divakaruni, A Dlasková, L Hlavatá, J Ježek, T Špacek, E Škobisová, U Brandt, RH Du, FF Wu, M Lu, X dong Shu, JH Ding, G Wu, G Hu, CM Duffy, H Xu, JP Nixon, DA Bernlohr, TA Butterick, D Duteil, C Chambon, F Ali, R Malivindi, J Zoll, S Kato, B Geny, P Chambon, D Metzger, C Duval, A Nègre-Salvayre, A Doglio, R Salvayre, L Pénicaud, L Casteilla, F Echeverría, M Ortiz, R Valenzuela, LA Videla, KS Echtay, JL Pakay, MB Jekabsons, AJ Lambert, M Portero-Otín, R Pamplona, AJ Vidal-Puig, S Wang, SJ Roebuck, V Eisner, RR Cupo, E Gao, G Csordás, WS Slovinsky, M Paillard, L Cheng, J Ibetti, SRW Chen, JK Chuprun, JB Hoek, WJ Koch, G Hajnóczky, A Elorza, B Hyde, HK Mikkola, OS 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Hou, Y Ding, T Zhang, C Shi, W Fu, Z Cai, F Yin, H Sancheti, E Cadenas, H Yoshitomi, K Yamazaki, I Tanaka, T Liu, SB Jin, C Ning, U Lendahl, M Nistér, SX Yu, CT Du, W Chen, QQ Lei, N Li, S Qi, XJ Zhang, GQ Hu, XM Deng, WY Han, YJ Yang, XX Yu, W Mao, A Zhong, P Schow, J Brush, SW Sherwood, G Pan, P Perret, O Peroni, YB Kim, XX Zheng, R Shen, CT Lin, JA Porco, HJ Zhang, W Zhao, S Venkataraman, MEC Robbins, GR Buettner, KC Kregel, LW Oberley, I Khvorostov, JS Hong, Y Oktay, L Vergnes, E Nuebel, PN Wahjudi, K Setoguchi, A Do, HJ Jung, JM McCaffery, IJ Kurland, K Reue, WNP Lee, CM Koehler, MA Teitell, K Zhang, Z Song, G Zheng, J Lyu, S Liu, J Huang, C Liu, D Xiang, M Xie, Q Zeng, M Zhou, PKH Tam, KSL Lam, B Huang, Y Liang, D Wu, Y Zhou, T Cai, J Xu, L Jiang, J Wu, Q Sun, R Zhu, A Ebner, T Haselgrübler, HJ Gruber, P Hinterdorfer Show less
Abstract Significance: Mitochondria are the energetic, metabolic, redox, and information signaling centers of the cell. Substrate pressure, mitochondrial network dynamics, and cristae morphology Show more
Abstract Significance: Mitochondria are the energetic, metabolic, redox, and information signaling centers of the cell. Substrate pressure, mitochondrial network dynamics, and cristae morphology state are integrated by the protonmotive force Δ p or its potential component, Δ Ψ , which are attenuated by proton backflux into the matrix, termed uncoupling. The mitochondrial uncoupling proteins (UCP1–5) play an eminent role in the regulation of each of the mentioned aspects, being involved in numerous physiological events including redox signaling. Recent Advances: UCP2 structure, including purine nucleotide and fatty acid (FA) binding sites, strongly support the FA cycling mechanism: UCP2 expels FA anions, whereas uncoupling is achieved by the membrane backflux of protonated FA. Nascent FAs, cleaved by phospholipases, are preferential. The resulting Δ p dissipation decreases superoxide formation dependent on Δ p . UCP-mediated antioxidant protection and its impairment are expected to play a major role in cell physiology and pathology. Moreover, UCP2-mediated aspartate, oxaloacetate, and malate antiport with phosphate is expected to alter metabolism of cancer cells. Critical Issues: A wide range of UCP antioxidant effects and participations in redox signaling have been reported; however, mechanisms of UCP activation are still debated. Switching off/on the UCP2 protonophoretic function might serve as redox signaling either by employing/releasing the extra capacity of cell antioxidant systems or by directly increasing/decreasing mitochondrial superoxide sources. Rapid UCP2 degradation, FA levels, elevation of purine nucleotides, decreased Mg 2+ , or increased pyruvate accumulation may initiate UCP-mediated redox signaling. Future Directions: Issues such as UCP2 participation in glucose sensing, neuronal (synaptic) function, and immune cell activation should be elucidated. Antioxid. Redox Signal. 29, 667–714. Show less
đź“„ PDF DOI: 10.1089/ars.2017.7225
mitochondria