Julio César Cárdenas

Associate Professor


J. Cesar Cardenas is a Medical Technologist in Morphophysiopathology and Cytodiagnosis and a PhD in Biomedical Sciences, both obtained at the University of Chile. He then completed a postdoc with Dr. Clara Franzini-Armstrong at the University of Pennsylvania (UPENN), determining the nuclear localization of the 1,4,5-trisphosphate-sensitive Ca2+ channel, InsP3R, using high-resolution electron microscopy and cryofracture. Motivated to better understand the physiological role of InsP3R, he joined the laboratory of Dr. Kevin Foskett also at UPENN, where he demonstrated for the first time that InsP3R-dependent basal Ca2+ signaling were essential for maintaining mitochondrial function.


Julio César Cárdenas

PUBLICATIONS

2015-pres

  • Ca2+ fluxes at Mitochondria-ER Contact Sites are a new target of senolysis in Therapy-Induced Senescence. Andrea Puebla-Huerta, Hernán Huerta, Camila Quezada, Pablo Morgado-Cáceres, César Casanova-Canelo, Sergio Linsambarth Osman Díaz-Rivera, José Alberto López-Domínguez, Sandra Rodríguez-López, Galdo Bustos, Eduardo Silva-Pavez, Alenka Lovy, Gabriel Quiroz, Catalina González-Seguel, Edison Salas-Huenuleo, Marcelo J. Kogan, Jordi Molgó, Armen Zakarian, José M. Villalba , Christian Gonzalez-Billault, Ulises Ahumada-Castro, J. César Cárdenas. BioRxiv 2024. doi.org/10.1101/2024.03.31.587471
  • Mitochondrial division inhibitor-1 (mdivi-1) induces extracellular matrix (ECM)-detachment of viable breast cancer cells by a DRP1-independent mechanism. Eduardo Silva-Pavez, Elizabeth Mendoza, Pablo Morgado, Ulises Ahumada-Castro, Galdo Bustos, Matías Kangme-Encalada, Amaia Lopez de Arbina, Andrea Puebla-Huerta, Felipe Muñoz, Lucas Cereceda, Manuel Varas-Godoy, Yessia Hidalgo, and J. César Cárdenas. Sci Rep. 2024 Jun 19;14(1):14178. doi: 10.1038/s41598-024-64228-9
  • Ketogenic diet administration later in life improves memory and regulates the synaptic cortical proteome through the cAMP/PKA signaling pathway in aging mice. Diego Acuña-Catalán, Samah Shah, Cameron Wehrfritz, Mitsunori Nomura, Alejandro Acevedo, Cristina Olmos, Gabriel Quiroz, Hernán Huerta, Joanna Bons, Estibaliz Ampuero, Ursula Wyneken, Magdalena Sanhueza, Felipe Arancibia, Darwin Contreras, Julio César Cárdenas, Bernardo Morales, Birgit Schilling, John C. Newman and Christian González-Billault. Cell Rep Med. 2024 Jun 18;5(6):101593. doi: 10.1016/j.xcrm.2024.101593
  • Functional selectivity of estradiol or phytoestrogens in membrane estrogen receptors of endothelial cells; fast NO production associated to vasorelaxation. Vicente Catalán, Pablo Sagredo, Williams Melgarejo, J. Cesar Cárdenas, Armen Zakarian, Verónica Donoso, J. Pablo Huidobro-Toro. Eur J Pharmacol. 2024 Jul 15;975:176636. doi: 10.1016/j.ejphar.2024.176636
  • Novel inositol 1,4,5-trisphosphate receptor inhibitor antagonizes hepatic stellate cell activation: a potential drug to treat liver fibrosis. Natalia Smith-Cortinez, Janette Heegsma, Masa Podunavac, Armen Zakarian, César Cardenas, Klaas Nico Faber. Cells. 2024 Apr 30;13(9):765. doi: 10.3390/cells13090765
  • Impact of platelet-released mitochondria transfer in the metabolic profiling and progression of metastatic MDA-MB-231 human triplenegative breast cancer cells. Lucas Cereceda, Cesar Cardenas, Maroun Khoury, Eduardo Silva-Pavez, Yessia Hidalgo. Front Cell Dev Biol. 2024 Jan 12;11:1324158. doi: 10.3389/fcell.2023.1324158
  • Sustained IP3-linked Ca2+ signaling promotes progression of triple negative breast cancer cells by regulating fatty acid metabolism. Filadi R, De Mario A, Audano M, Romani P, Pedretti S, Cardenas C, Dupont S, Mammucari C, Mitro N, Pizzo P. Front Cell Dev Biol. 11:1071037. 2023.
  • Necroptosis inhibition counteracts axonal degeneration, cognitive decline and key hallmarks of aging, promoting brain rejuvenation. Macarena S. Arrázola, Matías Lira, Gabriel Quiroz, Somya Iqbal, Samantha L Eaton, Rachel A Kline, Douglas J Lamont, Hernán Huerta, Gonzalo Ureta, Sebastián Bernales, J César Cárdenas, Waldo Cerpa, Thomas M. Wishart, Felipe A. Court. Aging Cell. 2023 May;22(5):e13814. doi: 10.1111/acel.13814
  • Unfolded protein response IRE1/XBP1 signaling is required for healthy mammalian brain aging. Cabral-Miranda F, Tamburini G, Martinez G, Ardiles AO, Medinas DB, Gerakis Y, Hung MD, Vidal R, Fuentealba M, Miedema T, Duran-Aniotz C, Diaz J, Ibaceta-Gonzalez C, Sabusap CM, Bermedo-Garcia F, Mujica P, Adamson S, Vitangcol K, Huerta H, Zhang X, Nakamura T, Sardi SP, Lipton SA, Kennedy BK, Henriquez JP, Cárdenas JC, Plate L, Palacios AG, Hetz C. EMBO J. 2022 Nov 17;41(22):e111952. doi: 10.15252/embj.2022111952
  • Balancing energy and protein homeostasis at ER-mitochondria contact sites. Carreras-Sureda A, Kroemer G, Cardenas JC, Hetz C.
    Sci Signal. 2022     Jul 5;15(741):eabm7524. doi:10.1126/scisignal.abm7524
  • A phenolic-rich extract from Ugni molinae berries reduces abnormal protein aggregation in a cellular model of Huntington’s disease. Rodrigo Pérez-Arancibia, Jose Luis Ordoñez, Alexis Rivas, Philippe Pihán, Alfredo Sagredo, Ulises Ahumada, Andrés Barriga, Ivette Seguel, César Cárdenas, Rene L. Vidal, Claudio Hetz, Carla Delporte. PLOS ONE 16(7): e0254834. 2021.
  • Directly Reprogrammed Human Neurons to Understand Age-Related Energy Metabolism Impairment and Mitochondrial Dysfunction in Healthy Aging and Neurodegeneration. Camila Gudenschwager, Isadora Chavez, Cesar Cardenas and Christian Gonzalez-Billault. Oxidative Medicine and Cellular Longevity, 5586052. 2021.
  • Keeping zombies alive: The ER-mitochondria Ca2+ transfer in cellular senescence. Ahumada-Castro U, Puebla-Huerta A, Cuevas-Espinoza V, Lovy A, Cardenas JC. Biochim Biophys Acta Mol Cell Res.1868(11):119099. 2021.
  • Cdkn1a transcript variant 2 is a marker of aging and cellular senescence. López-Domínguez JA, Rodríguez-López S, Ahumada-Castro U, Desprez PY , Konovalenko M, Laberge RM, Cárdenas C, Villalba JM & Campisi J. Aging. 13 (10):13380-13392. 2021
  • The ER-mitochondria Ca2 + signaling in cancer progression: Fueling the monster. Galdo Bustos, Ulises Ahumada-Castro, Eduardo Silva-Pavez, Andrea Puebla, Alenka Lovy, J. Cesar Cardenas. International Review of Cell and Molecular Biology. 363:49-121. 2021.
  • Scalable Total Synthesis, IP3R Inhibitory Activity of Desmethylxestospongin B, and Effect on Mitochondrial Function and Cancer Cell Survival. Maša Podunavac, Artur Mailyan, Jeffrey, J. Jackson, Alenka Lovy, Paula Farias, Hernan Huerta, Jordi Molgó, Cesar Cardenas, Armen Zakarian. Angew Chem Int Ed Engl. 60(20):11278-11282. 2021.
  • CD73 Ectonucleotidase Restrains CD8+ T Cell Metabolic Fitness and Anti-tumoral Activity. Briceño P, Rivas-Yañez E, Rosemblatt MV, Parra-Tello B, Farías P, Vargas L, Simon V, Cárdenas C, Lladser A, Salazar-Onfray F, Elorza AA, Rosemblatt M, Bono MR, Sauma D. Front Cell Dev Biol. 9:638037. 2021
  • Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition). Klionsky et al…Cardenas C., Autophagy. (1):1-382. 2021.
  • Ca2+ transfer to mitochondria: a spark of life in unexpected conditions. Silva-Pavez E, Ahumada-Castro U, Lovy A, Cárdenas JC. Mol Cell Oncol. 8(1):1839341. 2021.
  • In the right place at the right time: IP3 Receptor isoforms differentially controlling cellular metabolism Ulises Ahumada-Castro, Galdo Bustos, Eduardo Silva-Pavez, Andrea Puebla-Huerta, Alenka Lovy and César Cárdenas. Front Cell Dev Biol. 2;9:629522. 2021.
  • Inhibition of InsP3R with Xestospongin B reduces mitochondrial respiration and induces selective cell death in T cell acute lymphoblastic leukemia cells Pablo Cruz, Ulises Ahumada-Castro, Galdo Bustos, Jordi Molgó, Daniela Sauma, Alenka Lovy and César Cárdenas. Int J Mol Sci. 2021. 22(2):651.
  • Reduced mitochondrial function in idiopathic inflammatory myopathy derived myoblast is a metabolic adaptation to promote cell survival. Basualto-Alarcón, C., Urra, F.A., Bozán, M.F., Jaña, F., Trangulao, A., Bevilacqua, J.A., Cárdenas, C. PLOS ONE. 15(11):e0242443. 2020.
  • Concerted action of AMPK and sirtuin-1 induces mitochondrial fragmentation upon inhibition of Ca2+ transfer to mitochondria. Lovy, A., Ahumada-Castro, U., Bustos, G., Farias P., Molgo, J., and Cardenas C. Frontiers in Cell Developmental Biology. 8:378. 2020.
  • Cancer cells with defective oxidative phosphorylation require endoplasmic reticulum-to-mitochondria Ca2+ transfer for survival. Cardenas C., Lovy A., Silva-Pavez E., Urra F., Mizzoni C., Ahumada-Castro U., Bustos G., Jaňa F., Cruz P., Farias P., Mendoza E., Huerta H., Murgas P., Hunter M., Rios M., Cerda O., Georgakoudi I., Zakarian A., Molgó J., and Foskett JK. Science Signaling. 13(640):eaay1212. 2020.
  • SK channel activation potentiates auranofin-induced cell death in glio- and neuroblastoma cells. Krabbendam IE, Honrath B, Bothof L, Silva-Pavez E, Huerta H, Peñaranda Fajardo NM, Dekker F, Schmidt M, Culmsee C, Cárdenas C, Kruyt F, Dolga AM. Biochem Pharmacol. 171:113714. 2020.
  • Complex I and II Regulate Mitochondrial Ca2+ Homeostasis Independent of the Mitochondrial Membrane Potential. Jaňa, F., Bustos, G., Cruz, P., Lovy, A., Dong, Z., Madesh, M., and Cardenas, C. Mitochondrion.13;49:73-82. 2019
  • Non-canonical function of IRE1α determines mitochondria-associated endoplasmic reticulum composition to control calcium transfer and bioenergetics. Carreras-Sureda, A., Jaña, F., Ramos-Fernández, E., Urra, H., Van der Viett, A., Durand, S., Mortenson, D., Pihan, P., Gonzalez-Quiroz, M., Vicente, R., Inestrosa, N., Wiseman, L., Agostinis, P., Bultynck, G., Court, F., Kroemer, G., Cárdenas, C., and Hetz, C. Nature Cell Biology. 21(6):755-767. 2019
  • Antenatal melatonin modulates an enhanced antioxidant/pro-oxidant ratio in pulmonary hypertensive newborn sheep. Gonzalez-Candia A, Veliz M, Carrasco-Pozo C, Castillo RL, Cárdenas JC, Ebensperger G, Reyes RV, Llanos AJ, Herrera EA. Redox Biology. 22: 101128. 2019.
  • MTOR-independent autophagy induced by interrupted endoplasmic reticulum-mitochondrial Ca2+ communication: a dead end in cancer cells. Ahumada-Castro, U., Silva-Pavez, E., Pardo, E., Lovy, A., and Cárdenas, C. Autophagy. 15(2):358-361, 2019
  • FR58P1a; a new uncoupler of OXPHOS that inhibits migration in triple-negative breast cancer cells via Sirt1/AMPK/β1-integrin pathway. Urra FA, Muñoz F, Córdova-Delgado M, Ramírez MP, Peña-Ahumada B, Rios M, Cruz P, Ahumada-Castro U, Bustos G, Silva-Pavez E, Pulgar R, Morales D, Varela D, Millas-Vargas JP, Retamal E, Ramírez-Rodríguez O, Pessoa-Mahana H, Pavani M, Ferreira J, Cárdenas C, Araya-Maturana R. Scientific Report. 8(1):13190, 2018
  • Mitochondrial Regulation by Calcium as Basis of Neurodegeneration Associated to Aging. Müller, M., Ahumada-Castro, U., Gonzalez-Billault, C., Court, F.A., and Cárdenas, C. Frontiers in Neuroscience. 12:470, 2018
  • Hepatic Glutaminase activity and glutamine flux contributes to glucagon-stimulated gluconeogenesis and systemic glucose homeostasis. Miller, R.A., Shi, Y., Lu,W., Pirman, D.A., Jatkar, A., Blatnik, M., Wu, H., Cárdenas, C., Wan, M., Foskett, J.K., Park, J.O., Zhang, Y., Holland, W.L., Rabinowitz, J.D., Birnbaum, M.J. Nature Medicine. 24(4):518-524, 2018.
  • Mouse Tc17 cells display memory T cell-like traits. Flores-Santibáñez, F., Cuadra, B., Fernández, D., Rosemblatt, M., Núñez, S., Cruz, P., Gálvez-Cancino, F., Cárdenas, C., Lladser, A., Rosemblatt, M., Bono, M.R., and Sauma, D. Frontiers Immunology. 9:209, 2018.
  • Editorial: Inter- Organelle Calcium Communication in Cancer. Cardenas, C., Pinton, P., and Bultynck, G. Frontiers in Oncology. 8:14, 2018.
  • Calcium and Mitochondrial Metabolism in Cancer, a Novel Potential Target? Bustos, G., Cruz, P., Lovy, A., and Cárdenas C. Frontiers in Oncology. 7:199, 2017.
  • The mitochondrial complex(I)ty of cancer. Urra, FA., Muñoz, F., Lovy, A., Cárdenas, C. Frontiers in Oncology. 7:118, 2017.
  • Diabetic concentrations of Metformin inhibit platelet-mediated ovarian cancer cell progression. Erices, R., Cubillos, S., Aravena, R., Santoro, F., Marquez, M., Orellana, R., Ramírez, C., González, P., Fuenzalida, P., Bravo, ML., Oliva, B., Kato, S., Ibañez, C., Brañes, J., Bravo, E., Alonso, C., García, K., Arab, C., Torres, VA., Godoy, A., Pereira, J., Bustos, G., Cardenas, C., Cuello, MA., and Owen, GI. Oncotarget. 8 (13): 20865-20880, 2017.
  • The Paraguayan Rhinella toad venom: Implications in the traditional medicine and proliferation of breast cancer cells. Schmeda-Hirschmann, G., Gomez, CV., de Arias, AR., Burgos-Edwards, A., Alfonso J., Rolon, M., Brusquetti, F., Netto, F., Urra, FA., Cárdenas, C. J Ethnopharmacology. 199: 106–118, 2017.
  • Prolonged Activation of the Htr2b Serotonin Receptor Impairs Glucose Stimulated Insulin Secretion and Mitochondrial Function in MIN6 Cells. Cataldo, L., Mizgier, ML., Bravo, R., Jaña F., Cardenas, C., Llanos, P., Olmos PR., Galgani JE., Santos JL. and Cortés VA. PLOS One. 12(1):e0170213, 2017.
  • Antiproliferative activity and chemical composition of the venom from the Amazonian toad Rhinella marina (Anura: Bufonidae). Schmeda-Hirschmann, G., Quispe, C., Arana, GV., Theoduloz, C., Urra, FA. and Cárdenas C. Toxicon. 121:119-129, 2016.
  • InsP3R, the Calcium Whisperer: Maintaining Mitochondrial Function in Cancer. Lovy, A. Foskett, J.K. and Cardenas C. Molecular Cellular Oncology. 3(4):e1185563. 2016
  • Selective Vulnerability of Cancer Cells by Inhibition of Ca2+ Transfer from Endoplasmic Reticulum to Mitochondria. Cardenas, C., Muller, M, McNeal, A., Lovy, A., Jaňa, F., Bustos, G., Smith, N., Molgo, J., Diehl, A., Ridky, TW., and Foskett J.K. Cell Rep. 14(10):2313-24. 2016
  • Aminochrome induces dopaminergic neuronal dysfunction: a new animal model for Parkinson's disease. Herrera A., Muñoz, P., Paris, I., Díaz-Veliz, G., Mora, S., Inzunza, J., Hultenby, K., Cardenas, C., Jaña, F., Raisman-Vozari, R., Gysling, K., Abarca, J., Steinbusch, HW. and Segura-Aguilar, J. Cell Mol Life Sci. 73(18):3583-972016, 2016

RESEARCH LINES

Cancer metabolism

Mechanisms that regulate cell metabolism are a fundamental requirement for cell viability. Normal differentiated cells rely primarily on mitochondrial oxidative phosphorylation to generate the energy needed for cellular processes. In tumor cells, it has historically been assumed that mitochondrial metabolism is significantly diminished while aerobic glycolysis is enhanced so that it becomes the major ATP source to fuel cancer cell proliferation, a phenomenon known as the Warburg effect. Nevertheless, recent studies have shown that the mitochondrial tricarboxylic acid (TCA) cycle is both functional and essential for tumor growth, because provide the cells, in addition to energy, building blocks for the synthesis of macromolecules (proteins, lipids and nucleotides), and reducing equivalent which among other functions, regulate the redox state of the cell. Therefore, we focus our research in understand how mitochondrial activity is regulate and how we can modulate it in cancer cells. We discover that Ca2+ transfer from the endoplasmic reticulum (ER) mediate trough the inositol trisphosphate receptor (InsP3R) channel (InsP3R) to mitochondria maintain normal mitochondrial activity and the absence of this signal generate a bioenergetic crisis that induce selective cancer cell death. We demonstrate that Ca2+ transfer to mitochondria is essential to maintain the activity of pyruvate, α-ketoglutarate and isocitrate dehydrogenases, key rate limiting enzymes of the TCA cycle. In this scenario, we hypothesize that in the absence of Ca2+, tumor cells are unable to use glutamine and the TCA cycle to generate the building blocks needed to proliferate and maintain homeostasis. We expect that a deeper understanding of the regulation of mitochondria bioenergetics by InsP3R-released Ca2+ will result in the identification of new therapeutic targets.

Cellular senescence

By 2050, close to one fifth of the Chilean population will be over 60 years old, making Chile one of the countries with the highest number of elderly people. Aging is one of the main risk factors for cancer, heart and neurodegenerative diseases. Cellular senescence, an irreversible cell cycle arrest, play a big role in the decline of the regenerative potential and function of tissues, inflammation, and tumorigenesis in aged organisms. Thus, the identification, characterization, and pharmacological elimination of senescent cells have gained attention in the field of aging. Since cellular senescence is accompanied by change in metabolism and Ca2+ homeostasis, we aim to understand the role of mitochondria in the generation and maintenance of senescence cells and determine if the modulation of it activity can be use as a therapeutical tool.

Mitochondrial calcium in Alzheimer’s disease

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most frequent cause of dementia, affecting millions of people worldwide and still incurable. It is characterized clinically as a decline of intellectual and cognitive functions and irreversible memory loss as major features. Altered Ca2+ signaling and mitochondrial dysfunction are observed early in the development of the disease, long before the onset of measurable histopathology or cognitive deficits. However, the involvement of exaggerated Ca2+ signaling on mitochondrial dysfunction remain poorly understood. A molecular mechanism underlying exaggerated Ca2+ signaling is mediated in part by Ca2+ release from the endoplasmic reticulum (ER) through inositol 1,4,5-trisphosphate receptors (IP3R). IP3R are in close proximity with the mitochondrial Ca2+ uniporter (MCU), the ion channel responsible for sequestering Ca2+ into the mitochondrial matrix. We aim to study the relation InsP3R-MCU in an AD context and determine weather the normalization of Ca2+ signaling by decreasing IP3R activity will restore or prevent mitochondrial crisis and synaptic dysfunction in AD models.

Mitochondrial function in Dysferlinophathies

The dysferlinopathies include different muscular dystrophy phenotypes; all of which are autosomal recessive, and are consequence of mutations in the dysferlin gene (DYSF). Miyoshi’s distal myopathy (MM) and limb girdle muscular dystrophy 2B (LGMD2B), are the two more common dysferlinopathy phenotypes, and correspond to allelic disorders. The functionality of dysferlin in muscle cells is under active investigation. Pathogenesis of dysferlinopahy is attributed to impaired calcium-mediated muscle-membrane repair after normal stress injury. Abnormal mitochondria have been observed in myophaties like Pompe and Danon’s disease. Accumulation of damaged mitochondria usually reflects an autophagy malfunction, which generates a bioenergetic crisis sensed by AMPK, the master energy regulator of the cell. In the dysferlinopathies context is unknow weather the mitochondria are functional or not and which is the bioenergetic state of the cells. Thus, we aim to explore the signal pathway that regulate cellular bioenergetic in this pathophysiological context and determine is potential as a therapeutical target.

PROJECTS

Active:

2024-2026: ECOS-FONDECYT (France-Chile exchange grant) “Role of inositol 1,4,5-trisphosphate receptors in celular senescence” ECOS230006. (Principal Investigator)

2024-2027: FONDECYT (similar to a NIH R01) “IP3R disengagement from mitochondrial-endoplasmic reticulum contact sites (MERCS) activate mitochondrial retrograde signals that initiate the therapy induce senescence program”. N° 1240807. (Principal Investigator).

2020-2025: FONDAP (similar to a center grant) “Geroscience Center for Brain Health and Metabolism” N° 15150012. (Principal Investigator).

Completed:

2020-2023: FONDECYT “Constitutive InsP3R-mediated calcium transfer to the mitochondria as a specific vulnerability of senescent cells; effect on cancer relapse” N° 1200255. (Principal Investigator).

2022-2023: The Jain Foundation Inc grant “Ketosis ameliorates dysferlinopathy phenotype in bla/j mice by promoting mitochondrial function” (Principal Investigator).

2020-2022: The Jain Foundation Inc grant “Ketogenic diet ameliorates dysferlinopathy phenotype by promoting mitochondrial function in in vitro and in vivo models of the disease” (Principal Investigator).

2018-2021: FONDECYT “New mitochondria-targeted anti-tumor compounds: Synthesis of anti-proliferative and anti-migratory phosphonium and pyridinium salts derived from acylpolyphenols” N° 1180069 (Co- Investigator).

2016-2019: FONDECYT “Mitochondrial uptake of constitutive InsP3R-released Ca2+ is essential to maintain mitochondrial metabolism and sustain breast cancer cell migration, invasion and metastasis”. N°1160332. (Principal Investigator).

2015-2018: FONDECYT “Autophagy as a possible pathophysiological mechanism in dysferlinopathy” N° 1151383. (Co- Investigator)

2014-2017: FONDECYT “Regulation of skeletal muscle atrophy and autophagy by polycystin 2” N° 1140908. (Co-Investigator).

2014-2017: Supporting the development of research projects between Chile and the United States “Gene therapy strategy to target the unfolded protein response (UPR) in ALS”. N° USA2013-0003. ( Co-Investigator).

2012-2015: FONDECYT “Mitochondrial Ca2+ uptake mediated by InsP3 receptors is required to maintain cancer cell bioenergetics. Its inhibition results in selective cancer cell death.” N° 1120443. (Principal Investigator).

2012: FONDEQUIP “Cellular Bioenergetics” N°EQM120032. (Principal Investigator).

TEAM

Andrea Puebla-Huerta, , Lab Manager.

Osman Diaz, Research Assistant.

Loreto Araos, Research Assistant.

Donato Garrido, Research Assistant.

Sergio Linsambarth, Postdoc.

Hernan Huerta, Postdoc.

Pablo Morgado, PhD student in Biochemistry from Universidad de Chile.

Cesar Casanova PhD student in Neurobiology from Universidad Mayor.

Alejandra Lopez-Moroni, PhD student in Neurobiology from Universidad Mayor.

NETWORK

Nacional

Dr. Jorge Bevilacqua, Hospital Jose Joaquin Aguirre, Universidad de Chile, Santiago Chile

Dr. Felipe Salech, School of Medicine, Universidad de Chile, Santiago Chile

Dr. Ute Woehlbier, Center for Integrative Biology, Universidad Mayor, Santiago, Chile

Dr. Daniela Sauma, School of Science, Universidad de Chile, Santiago Chile

Dr. Patricia Luz-Crawford, Centro de Investigación e Innovación Biomédica, Facultad de Medicina, Universidad de los Andes

Dr. Diego Garcia, School of Medicine, Universidad de Chile, Santiago Chile

Dr. Alejandro Godoy, CEBICEM, Universidad San Sebastian

Dr. Juan Garcia-Huidobro, Facultad de Quimica y Biologia, Usach.

Internacional

Dr. Kevin Foskett, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA.

Dr. Armen Zakarian, Department of Chemistry, University of California, Santa Barbara, USA.

Dr. Mariano Viapiano, Neuroscience and Physiology department, Upstate Medical University. USA.

Dr. David Bernard, Cancer Research Centre of Lyon, University of Lyon. France.

Dr Paola Pizzo, department of Biomedical Science, University of Padova.

Dr. Tito Cali, department of Biomedical Science, University of Padova.

Dr. Amalia Dolga, Faculty of Science and Engineering, Groningen University, Groningen, Netherland

Dr. Jordi Molgo, Institute de Neurobiologie Alfred Fessard, CNRS, Gif-sur-Yvette, France

Dr. Jimmy Crott, USDA Human Nutrition Research Center on Aging, Tufts University, Boston, USA