Professor Alberto Sanz Montero

Wellcome Trust Senior Research Fellow (Molecular Biosciences)

email: Alberto.SanzMontero@glasgow.ac.uk

Biography

I have dedicated my career to understanding how and why we age and to the development of therapies to prevent, delay or reverse ageing and age-related diseases. In 2006, I obtained my PhD in Biology from Complutense University of Madrid, after receiving additional training in Poland and the United States. After my PhD, I moved to Finland as a postdoc supported by a long-term EMBO fellowship.

In 2010, I was awarded a Starting Grant from the ERC to establish my laboratory and was nominated as a Research Academy Fellow by the Finnish Academy. In 2014, I was recruited by Newcastle University, where I was promoted to full professor in 2019. In 2018, I received a Senior Research Fellowship from Wellcome.

In 2020, I joined the University of Glasgow as a Lord Kelvin/Adam Smith Professor. My laboratory is funded by the BBSRC, Wellcome and the University of Glasgow, and our work has been published in the prestigious journals in the field such as Cell Metabolism, PNAS, Nature Communications or Redox Biology.

Our laboratory is interested in understanding how information flows between the mitochondria and the rest of the cell, the way mitochondrial signals contribute to cellular homeostasis and why damaged mitochondria accumulate during ageing. To achieve our ultimate goal of helping people live healthier for longer, we have established strategic collaborations with other national and international research groups. If you are interested in collaborating or interacting with us, please don’t hesitate to contact us.

Research interests

How and why we age are two of the most intriguing biological questions which remain unanswered. Ageing is the major issue public health services around the globe are facing. Understanding ageing requires identification of the biological processes that affect it. One of the hallmarks of ageing is the accumulation of defective mitochondria that produce more mitochondrial Reactive Oxygen Species (mtROS). ROS are both a toxic by-product of metabolism and essential cellular messengers. Our laboratory and others have shown that mtROS are essential regulators of lifespan and that by boosting mtROS production, it is possible to improve animal health and allow them to live longer.

We do not know mechanistically how mtROS regulate longevity, and therefore, cannot currently use them as a therapeutic tool to extend healthspan. Although mtROS were described decades ago, we are only just starting to understand the role they play in cellular signalling and how they control essential cellular processes such as differentiation, proliferation and cell death. Our laboratory aims to fill these gaps and provide new and relevant knowledge which would allow the use mtROS as a therapeutical tool to prevent, delay or reverse ageing and age-related diseases. We work on four different areas in collaboration with national and international partners:

How is information exchanged between the mitochondrion and the rest of the cell? Why is this interrupted during ageing?
Where and how are mtROS produced within mitochondria? How does redox signalling contribute to cellular homeostasis?
What are the genetic and epigenetic mechanisms that underlie the accumulation of damaged mitochondria during ageing?
Development of technologies allowing the manipulation of mitochondrial function to extend healthspan and prevent age-related diseases.

Research groups

Publications

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Number of items: 58.

2023

Vitale, M., Sanz, A. and Scialò, F. (2023) Mitochondrial redox signaling: a key player in aging and disease. Aging, (doi: 10.18632/aging.204659) (PMID:37052982) (Early Online Publication)

Castejon-Vega, B. , Cordero, M. D. and Sanz, A. (2023) How the disruption of mitochondrial redox signalling contributes to ageing. Antioxidants, 12(4), 831. (doi: 10.3390/antiox12040831) (PMID:37107206) (PMCID:PMC10135186)

2022

Kataura, T. et al. (2022) Autophagy promotes cell survival by maintaining NAD levels. Developmental Cell, 57(22), 2584-2598.e11. (doi: 10.1016/j.devcel.2022.10.008) (PMID:36413951) (PMCID:36413951)

Graham, C. et al. (2022) Mitochondrial ROS signalling requires uninterrupted electron flow and is lost during ageing in flies. GeroScience, 44(4), pp. 1961-1974. (doi: 10.1007/s11357-022-00555-x) (PMID:35355221) (PMCID:PMC9616974)

2021

Castejón-Vega, B. et al. (2021) L-arginine ameliorates defective autophagy in GM2 gangliosidoses by mTOR modulation. Cells, 10(11), 3122. (doi: 10.3390/cells10113122)

Navas, P. and Sanz, A. (2021) Editorial: "Mitochondrial Coenzyme Q Homeostasis: signalling, respiratory chain stability and diseases.". Free Radical Biology and Medicine, 169, pp. 12-13. (doi: 10.1016/j.freeradbiomed.2021.04.005) (PMID:33845159)

Scialo, F. and Sanz, A. (2021) Coenzyme Q redox signalling and longevity. Free Radical Biology and Medicine, 164, pp. 187-205. (doi: 10.1016/j.freeradbiomed.2021.01.018) (PMID:33450379)

Navarro-Pando, J. M. et al. (2021) Inhibition of the NLRP3 inflammasome prevents ovarian aging. Science Advances, 7(1), eabc7409. (doi: 10.1126/sciadv.abc7409) (PMID:33523841) (PMCID:PMC7775749)

Klionsky, D. J. et al. (2021) Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition). Autophagy, 17(1), pp. 1-382. (doi: 10.1080/15548627.2020.1797280) (PMID:33634751) (PMCID:PMC7996087)

2020

Scialò, F., Sriram, A., Stefanatos, R. , Spriggs, R. V., Loh, S. H.Y., Martins, L. M. and Sanz, A. (2020) Mitochondrial complex I derived ROS regulate stress adaptation in Drosophila melanogaster. Redox Biology, 32, 101450. (doi: 10.1016/j.redox.2020.101450) (PMID:32146156) (PMCID:PMC7264463)

2019

Gubina, N. et al. (2019) Essential physiological differences characterize short- and long-lived strains of Drosophila melanogaster. Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 74(12), pp. 1835-1843. (doi: 10.1093/gerona/gly143) (PMID:29945183)

Pulli, I. et al. (2019) Sphingosine kinase 1 overexpression induces MFN2 fragmentation and alters mitochondrial matrix Ca2+ handling in HeLa cells. Biochimica et Biophysica Acta: Molecular Cell Research, 1866(9), pp. 1475-1486. (doi: 10.1016/j.bbamcr.2019.06.006) (PMID:31220477)

2018

Thompson, K. et al. (2018) OXA 1L mutations cause mitochondrial encephalopathy and a combined oxidative phosphorylation defect. EMBO Molecular Medicine, 10(11), e9060. (doi: 10.15252/emmm.201809060) (PMID:30201738) (PMCID:PMC6220311)

Stefanatos, R. and Sanz, A. (2018) The role of mitochondrial ROS in the aging brain. FEBS Letters, 592(5), pp. 743-758. (doi: 10.1002/1873-3468.12902) (PMID:29106705)

Carroll, B. et al. (2018) Oxidation of SQSTM1/p62 mediates the link between redox state and protein homeostasis. Nature Communications, 9, 256. (doi: 10.1038/s41467-017-02746-z) (PMID:29343728) (PMCID:PMC5772351)

2017

Scialò, F., Fernández-Ayala, D. J. and Sanz, A. (2017) Role of mitochondrial reverse electron transport in ROS signaling: potential roles in health and disease. Frontiers in Physiology, 8, 428. (doi: 10.3389/fphys.2017.00428) (PMID:28701960) (PMCID:PMC548615)

2016

Antoniewski, C., Scialo, F., Sriram, A., Stefanatos, R. and Sanz, A. (2016) Practical recommendations for the use of the GeneSwitch Gal4 system to knock-down genes in Drosophila melanogaster. PLoS ONE, 11(8), e0161817. (doi: 10.1371/journal.pone.0161817) (PMID:27570965) (PMCID:PMC5003377)

Sanz, A. (2016) Mitochondrial reactive oxygen species: Do they extend or shorten animal lifespan? Biochimica et Biophysica Acta: Bioenergetics, 1857(8), pp. 1116-1126. (doi: 10.1016/j.bbabio.2016.03.018) (PMID:26997500)

Scialò, F. et al. (2016) Mitochondrial ROS produced via reverse electron transport extend animal lifespan. Cell Metabolism, 23(4), pp. 725-734. (doi: 10.1016/j.cmet.2016.03.009) (PMID:27076081) (PMCID:PMC4835580)

2015

Gerhold, J. M., Cansiz-Arda, Ş., Lõhmus, M., Engberg, O., Reyes, A., van Rennes, H., Sanz, A. , Holt, I. J., Cooper, H. M. and Spelbrink, J. N. (2015) Human mitochondrial DNA-protein complexes attach to a cholesterol-rich membrane structure. Scientific Reports, 5, 15292. (doi: 10.1038/srep15292) (PMID:26478270) (PMCID:PMC4609938)

Rovenko, B. M., Kubrak, O. I., Gospodaryov, D. V., Yurkevych, I. S., Sanz, A., Lushchak, O. V. and Lushchak, V. I. (2015) Restriction of glucose and fructose causes mild oxidative stress independently of mitochondrial activity and reactive oxygen species in Drosophila melanogaster. Comparative Biochemistry and Physiology. Part A: Molecular and Integrative Physiology, 187, pp. 27-39. (doi: 10.1016/j.cbpa.2015.04.012) (PMID:25941153)

Syrjänen, L., Valanne, S., Kuuslahti, M., Tuomela, T., Sriram, A., Sanz, A., Jacobs, H. T., Rämet, M. and Parkkila, S. (2015) β carbonic anhydrase is required for female fertility in Drosophila melanogaster. Frontiers in Zoology, 12, 19. (doi: 10.1186/s12983-015-0111-3) (PMID:26300950) (PMCID:PMC4546311)

Rovenko, B. M., Kubrak, O. I., Gospodaryov, D. V., Perkhulyn, N. V., Yurkevych, I. S., Sanz, A., Lushchak, O. V. and Lushchak, V. I. (2015) High sucrose consumption promotes obesity whereas its low consumption induces oxidative stress in Drosophila melanogaster. Journal of Insect Physiology, 79, pp. 42-54. (doi: 10.1016/j.jinsphys.2015.05.007) (PMID:26050918)

Rovenko, B. M., Perkhulyn, N. V., Gospodaryov, D. V., Sanz, A., Lushchak, O. V. and Lushchak, V. I. (2015) High consumption of fructose rather than glucose promotes a diet-induced obese phenotype in Drosophila melanogaster. Comparative Biochemistry and Physiology. Part A: Molecular and Integrative Physiology, 180, pp. 75-85. (doi: 10.1016/j.cbpa.2014.11.008) (PMID:25461489)

Scialò, F., Sriram, A., Naudí, A., Ayala, V., Jové, M., Pamplona, R. and Sanz, A. (2015) Target of rapamycin activation predicts lifespan in fruit flies. Cell Cycle, 14(18), pp. 2949-2958. (doi: 10.1080/15384101.2015.1071745) (PMID:26259964) (PMCID:PMC4630862)

2014

Mallikarjun, V., Sriram, A., Scialo, F. and Sanz, A. (2014) The interplay between mitochondrial protein and iron homeostasis and its possible role in ageing. Experimental Gerontology, 56, pp. 123-134. (doi: 10.1016/j.exger.2013.12.015) (PMID:24394155)

2013

Kemppainen, K. K. et al. (2013) Expression of alternative oxidase in Drosophila ameliorates diverse phenotypes due to cytochrome oxidase deficiency. Human Molecular Genetics, 23(8), pp. 2078-2093. (doi: 10.1093/hmg/ddt601) (PMID:24293544) (PMCID:PMC3959817)

Scialo, F., Mallikarjun, V., Stefanatos, R. and Sanz, A. (2013) Regulation of lifespan by the mitochondrial electron transport chain: reactive oxygen species-dependent and reactive oxygen species-independent mechanisms. Antioxidants and Redox Signaling, 19(16), pp. 1953-1969. (doi: 10.1089/ars.2012.4900)

2012

Chen, S., Oliveira, M. T., Sanz, A., Kemppainen, E., Fukuoh, A., Schlicht, B., Kaguni, L. S. and Jacobs, H. T. (2012) A cytoplasmic suppressor of a nuclear mutation affecting mitochondrial functions in Drosophila. Genetics, 192(2), pp. 483-493. (doi: 10.1534/genetics.112.143719) (PMID:22851652) (PMCID:PMC3454878)

Stefanatos, R., Sriram, A., Kiviranta, E., Mohan, A., Ayala, V., Jacobs, H. T., Pamplona, R. and Sanz, A. (2012) dj-1β regulates oxidative stress, insulin-like signaling and development in Drosophila melanogaster. Cell Cycle, 11(20), pp. 3876-3886. (doi: 10.4161/cc.22073) (PMID:22983063) (PMCID:PMC349582)

2011

Stefanatos, R. and Sanz, A. (2011) Mitochondrial complex I: A central regulator of the aging process. Cell Cycle, 10(10), pp. 1528-1532. (doi: 10.4161/cc.10.10.15496)

2010

Tarnopolsky, M. A. et al. (2010) Mitochondrial DNA mutations induce mitochondrial dysfunction, apoptosis and sarcopenia in skeletal muscle of mitochondrial DNA mutator mice. PLoS ONE, 5(7), e11468. (doi: 10.1371/journal.pone.0011468) (PMID:20628647) (PMCID:PMC2898813)

Sanz, A., Fernández-Ayala, D. J.M., Stefanatos, R. K. and Jacobs, H. T. (2010) Mitochondrial ROS production correlates with, but does not directly regulate lifespan in drosophila. Aging, 2(4), pp. 200-223. (doi: 10.18632/aging.100137) (PMID:20453260) (PMCID:PMC2880708)

Sanz, A., Stefanatos, R. and McIlroy, G. (2010) Production of reactive oxygen species by the mitochondrial electron transport chain in Drosophila melanogaster. Journal of Bioenergetics and Biomembranes, 42(2), pp. 135-142. (doi: 10.1007/s10863-010-9281-z) (PMID:20300811)

Sanz., A. et al. (2010) Expression of the yeast NADH dehydrogenase Ndi1 in Drosophila confers increased lifespan independently of dietary restriction. Proceedings of the National Academy of Sciences of the United States of America, 107(20), pp. 9105-9110. (doi: 10.1073/pnas.0911539107) (PMID:20435911) (PMCID:PMC2889079)

2009

Fernandez-Ayala, D.J.M. et al. (2009) Expression of the ciona intestinalis alternative oxidase (aox) in drosophila complements defects in mitochondrial oxidative phosphorylation. Cell Metabolism, 9(5), pp. 449-460. (doi: 10.1016/j.cmet.2009.03.004)

Sanz, A., Barja, G., Pamplona, R. and Leeuwenburgh, C. (2009) Free radicals and mammalian aging. In: Jacob, C. and Winyard, P. (eds.) Redox Signaling and Regulation in Biology and Medicine. Wiley, pp. 433-472. ISBN 9783527319251 (doi: 10.1002/9783527627585.ch19)

2008

Sanz, A. and Stefanatos, R. K.A. (2008) The mitochondrial free radical theory of aging: a critical view. Current Aging Science, 1(1), pp. 10-21. (doi: 10.2174/1874609810801010010)

2007

Ayala, V., Naudi, A., Sanz Montero, A., Caro, P., Portero-Otin, M., Barja, G. and Pamplona, R. (2007) Dietary protein restriction decreases oxidative protein damage, peroxidizability index, and mitochondrial complex I content in rat liver. Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 62(4), pp. 352-360. (doi: 10.1093/gerona/62.4.352)

Caro, P., Gómez, J., Sanz, A., Portero-Otín, M., Pamplona, R. and Barja, G. (2007) Effect of graded corticosterone treatment on aging-related markers of oxidative stress in rat liver mitochondria. Biogerontology, 8(1), pp. 1-11. (doi: 10.1007/s10522-006-9026-x)

Sanz., A. , Hiona, A., Kujoth, G., Seo, A., Hofer, T., Kouwenhoven, E., Kalani, R., Prolla, T., Barja, G. and Leeuwenburgh, C. (2007) Evaluation of sex differences on mitochondrial bioenergetics and apoptosis in mice. Experimental Gerontology, 42(3), pp. 173-182. (doi: 10.1016/j.exger.2006.10.003)

2006

Sanz., A., Gómez, J., Caro, P. and Barja, G. (2006) Carbohydrate restriction does not change mitochondrial free radical generation and oxidative DNA damage. Journal of Bioenergetics and Biomembranes, 38(5-6), pp. 327-333. (doi: 10.1007/s10863-006-9051-0) (PMID:17136610)

Caro, P., Sanz, A., Gómez, J. and Barja, G. (2006) La restricción de metionina en la dieta disminuye el estrés oxidativo en mitocondrias de corazón = Methionine dietary restriction decreases oxidative stress in heart mitochondria. Revista Española de Geriatría y Gerontología, 41(6), pp. 334-339. (doi: 10.1016/S0211-139X(06)72985-7)

Sanz, A., Caro, P., Ayala, V., Portero-Otin, M., Pamplona, R. and Barja, G. (2006) Methionine restriction decreases mitochondrial oxygen radical generation and leak as well as oxidative damage to mitochondrial DNA and proteins. FASEB Journal, 20(8), pp. 1064-1073. (doi: 10.1096/fj.05-5568com) (PMID:16770005)

Sanz, A., Caro, P., Gómez, J. and Barja, G. (2006) Testing the vicious cycle theory of mitochondrial ROS production: effects of H2O2 and cumene hydroperoxide treatment on heart mitochondria. Journal of Bioenergetics and Biomembranes, 38(2), pp. 121-127. (doi: 10.1007/s10863-006-9011-8) (PMID:16841200)

Sanz, A. and Barja, G. (2006) Estimation of the rate of production of oxygen radicals by mitochondria. In: Conn, P. M. (ed.) Handbook of Models for Human Aging. Elsevier, pp. 183-189. ISBN 9780123693914 (doi: 10.1016/B978-012369391-4/50017-5)

Sanz, A., Pamplona, R. and Barja, G. (2006) Is the mitochondrial free radical theory of aging intact? Antioxidants and Redox Signaling, 8(3-4), pp. 582-599. (doi: 10.1089/ars.2006.8.582) (PMID:16677102)

Sorensen, M., Sanz, A., Gómez, J., Pamplona, R., Portero-Otín, M., Gredilla, R. and Barja, G. (2006) Effects of fasting on oxidative stress in rat liver mitochondria. Free Radical Research, 40(4), pp. 339-347. (doi: 10.1080/10715760500250182) (PMID:1029-2470)

2005

Pamplona, R., Portero-Otín, M., Sanz, A., Ayala, V., Vasileva, E. and Barja, G. (2005) Protein and lipid oxidative damage and Complex I content are lower in the brain of budgerigar and canaries than in mice. Relation to aging rate. AGE, 27(4), pp. 267-280. (doi: 10.1007/s11357-005-4562-x) (PMID:23598660) (PMCID:PMC3455889)

Sanz, A., Caro, P., Ibañez, J., Gómez, J., Gredilla, R. and Barja, G. (2005) Dietary restriction at old age lowers mitochondrial oxygen radical production and leak at Complex I and oxidative DNA damage in rat brain. Journal of Bioenergetics and Biomembranes, 37(2), pp. 83-90. (doi: 10.1007/s10863-005-4131-0) (PMID:15906153)

Sanz., A., Gredilla, R., Pamplona, R., Portero-Otin, M., Vara, E., Tresguerres, J. A. F. and Barja, G. (2005) Effect of insulin and growth hormone on rat heart and liver oxidative stress in control and caloric restricted animals. Biogerontology, 6(1), pp. 15-26. (doi: 10.1007/s10522-004-7380-0) (PMID:15834660)

Sanz., A., Gredilla, R., Pamplona, R., Portero-Ottin, M., Vara, E., Tresguerres, J. A. F. and Barja, G. (2005) Effect of insulin and growth hormone on rat heart and liver oxidative stress in control and caloric restricted animals. Biogerontology, 6(1), pp. 15-26. (doi: 10.1007/s10522-004-7380-0) (PMID:15834660)

2004

Sanz, A., Caro, P. and Barja, G. (2004) Protein restriction without strong caloric restriction decreases mitochondrial oxygen radical production and oxidative DNA damage in rat liver. Journal of Bioenergetics and Biomembranes, 36(6), pp. 545-552. (doi: 10.1007/s10863-004-9001-7) (PMID:15692733)

Pamplona, R., Portero-Otın, M., Sanz, A., Requena, J. and Barja, G. (2004) Modification of the longevity-related degree of fatty acid unsaturation modulates oxidative damage to proteins and mitochondrial DNA in liver and brain. Experimental Gerontology, 39(5), pp. 725-733. (doi: 10.1016/j.exger.2004.01.006) (PMID:15130667)

Sanz Montero, A., Gredilla, R., Herrero, A. and Barja de Quiroga, G. (2004) Efecto del peróxido de hidrógeno en la producción mitocondr de radicales libres en relación con el envejecimiento = Effect of hydrogen peroxide on mitochondrial free radical production in relation to ageing. Revista Española de Geriatría y Gerontología, 39(1), pp. 29-34. (doi: 10.1016/S0211-139X(04)74928-8)

2002

Sanz, A., Bartke, A. and Barja, G. (2002) Long-lived Ames dwarf mice: Oxidative damage to mitochondrial DNA in heart and brain. AGE, 25(3), pp. 119-122. (doi: 10.1007/s11357-002-0010-3) (PMID:23604907) (PMCID:PMC3455243)

López-Torres, M., Gredilla, R., Sanz, A. and Barja, G. (2002) Influence of aging and long-term caloric restriction on oxygen radical generation and oxidative DNA damage in rat liver mitochondria. Free Radical Biology and Medicine, 32(9), pp. 882-889. (doi: 10.1016/S0891-5849(02)00773-6) (PMID:11978489)

2001

Gredilla, R., Sanz, A., Lopez-Torres, M. and Barja, G. (2001) Caloric restriction decreases mitochondrial free radical generation at complex I and lowers oxidative damage to mitochondrial DNA in the rat heart. FASEB Journal, 15(9), pp. 1589-1591. (doi: 10.1096/fj.00-0764fje) (PMID:11427495)

This list was generated on Thu Apr 18 14:13:45 2024 BST.

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