Nerea is a Postdoctoral Scholar at Dr. Joseph Wu's lab. She earned her Bachelor's degree in Biochemistry at Universidad Complutense de Madrid (Spain). She was in an exchange program at the University of Saskatchewan (Canada) where she completed her Honours Thesis project on the Regulation of the Metastasis Suppressor Protein CREB3L1 in Dr. Deborah H Anderson's lab. She received her Masters' degree at Universidad de Alcalá (Spain) working at Dr. Isabel Liste Noya's lab on The role of p27Kip1 in the pluripotency and differentiation of dopaminergic neurons. She obtained her Ph.D. in Dr. Naweed Syed's lab studying the Cellular and molecular mechanisms underlying anesthetic-induced cytotoxicity, and their impact on learning and memory.

Honors & Awards

  • ATRAC postdoctoral fellowship, American Heart Association (Sept 2022)

Professional Education

  • BSc, Universidad Complutense de Madrid, University of Saskatchewan, Biochemistry, Cancer (2016)
  • MSc, Universidad de Alcalá, Stem cells, Parkinson's Disease (2017)
  • PhD, University of Calgary, Anesthetics, neuroscience (2021)

Stanford Advisors

All Publications

  • Generation of two iPSC lines from long QT syndrome patients carrying SNTA1 variants. Stem cell research Jimenez-Tellez, N., Vera, C. D., Yildirim, Z., Vicente Guevara, J., Zhang, T., Wu, J. C. 2022; 66: 103003


    Long QT syndrome (LQTS) is an inherited cardiovascular disorder characterized by electrical conduction abnormalities leading to arrhythmia, fainting, seizures, and an increased risk of sudden death. There are over 15 genes involved in causing LQTS, including SNTA1. Here we generated two human-induced pluripotent stem cell (iPSC) lines from two LQT patients carrying a missense mutation in SNTA1 (c.1088A>C). Both lines showed normal morphological properties, expressed pluripotency markers, showed a normal karyotype profile, and had the ability to differentiate into the three germ layers, making them a valuable tool to model LQTS to investigate the pathological mechanisms related to this SNTA1 variant.

    View details for DOI 10.1016/j.scr.2022.103003

    View details for PubMedID 36528013

  • Dexmedetomidine does not compromise neuronal viability, synaptic connectivity, learning and memory in a rodent model SCIENTIFIC REPORTS Jimenez-Tellez, N., Iqbal, F., Pehar, M., Casas-Ortiz, A., Rice, T., Syed, N. 2021; 11 (1): 16153


    Recent animal studies have drawn concerns regarding most commonly used anesthetics and their long-term cytotoxic effects, specifically on the nervous tissue. It is therefore imperative that the search continues for agents that are non-toxic at both the cellular and behavioural level. One such agent appears to be dexmedetomidine (DEX) which has not only been found to be less neurotoxic but has also been shown to protect neurons from cytotoxicity induced by other anesthetic agents. However, DEX's effects on the growth and synaptic connectivity at the individual neuronal level, and the underlying mechanisms have not yet been fully resolved. Here, we tested DEX for its impact on neuronal growth, synapse formation (in vitro) and learning and memory in a rodent model. Rat cortical neurons were exposed to a range of clinically relevant DEX concentrations (0.05-10 µM) and cellular viability, neurite outgrowth, synaptic assembly and mitochondrial morphology were assessed. We discovered that DEX did not affect neuronal viability when used below 10 µM, whereas significant cell death was noted at higher concentrations. Interestingly, in the presence of DEX, neurons exhibited more neurite branching, albeit with no differences in corresponding synaptic puncta formation. When rat pups were injected subcutaneously with DEX 25 µg/kg on postnatal day 7 and again on postnatal day 8, we discovered that this agent did not affect hippocampal-dependent memory in freely behaving animals. Our data demonstrates, for the first time, the non-neurotoxic nature of DEX both in vitro and in vivo in an animal model providing support for its utility as a safer anesthetic agent. Moreover, this study provides the first direct evidence that although DEX is growth permissive, causes mitochondrial fusion and reduces oxygen reactive species production, it does not affect the total number of synaptic connections between the cortical neurons in vitro.

    View details for DOI 10.1038/s41598-021-95635-x

    View details for Web of Science ID 000683506200054

    View details for PubMedID 34373548

    View details for PubMedCentralID PMC8352930

  • A synthetic peptide rescues rat cortical neurons from anesthetic-induced cell death, perturbation of growth and synaptic assembly SCIENTIFIC REPORTS Iqbal, F., Pehar, M., Thompson, A. J., Azeem, U., Jahanbakhsh, K., Jimenez-Tellez, N., Sabouny, R., Batool, S., Syeda, A., Chow, J., Machiraju, P., Shutt, T., Yusuf, K., Shearer, J., Rice, T., Syed, N. 2021; 11 (1): 4567


    Anesthetics are deemed necessary for all major surgical procedures. However, they have also been found to exert neurotoxic effects when tested on various experimental models, but the underlying mechanisms remain unknown. Earlier studies have implicated mitochondrial fragmentation as a potential target of anesthetic-induced toxicity, although clinical strategies to protect their structure and function remain sparse. Here, we sought to determine if preserving mitochondrial networks with a non-toxic, short-life synthetic peptide-P110, would protect cortical neurons against both inhalational and intravenous anesthetic-induced neurotoxicity. This study provides the first direct and comparative account of three key anesthetics (desflurane, propofol, and ketamine) when used under identical conditions, and demonstrates their impact on neonatal, rat cortical neuronal viability, neurite outgrowth and synaptic assembly. Furthermore, we discovered that inhibiting Fis1-mediated mitochondrial fission reverses anesthetic-induced aberrations in an agent-specific manner. This study underscores the importance of designing mitigation strategies invoking mitochondria-mediated protection from anesthetic-induced toxicity in both animals and humans.

    View details for DOI 10.1038/s41598-021-84168-y

    View details for Web of Science ID 000626620700008

    View details for PubMedID 33633281

    View details for PubMedCentralID PMC7907385

  • SS-31 Peptide Reverses the Mitochondrial Fragmentation Present in Fibroblasts From Patients With DCMA, a Mitochondrial Cardiomyopathy FRONTIERS IN CARDIOVASCULAR MEDICINE Machiraju, P., Wang, X., Sabouny, R., Huang, J., Zhao, T., Iqbal, F., King, M., Prasher, D., Lodha, A., Jimenez-Tellez, N., Ravandi, A., Argiropoulos, B., Sinasac, D., Khan, A., Shutt, T. E., Greenway, S. C. 2019; 6: 167


    We used patient dermal fibroblasts to characterize the mitochondrial abnormalities associated with the dilated cardiomyopathy with ataxia syndrome (DCMA) and to study the effect of the mitochondrially-targeted peptide SS-31 as a potential novel therapeutic. DCMA is a rare and understudied autosomal recessive disorder thought to be related to Barth syndrome but caused by mutations in DNAJC19, a protein of unknown function localized to the mitochondria. The clinical disease is characterized by 3-methylglutaconic aciduria, dilated cardiomyopathy, abnormal neurological development, and other heterogeneous features. Until recently no effective therapies had been identified and affected patients frequently died in early childhood from intractable heart failure. Skin fibroblasts from four pediatric patients with DCMA were used to establish parameters of mitochondrial dysfunction. Mitochondrial structure, reactive oxygen species (ROS) production, cardiolipin composition, and gene expression were evaluated. Immunocytochemistry with semi-automated quantification of mitochondrial structural metrics and transmission electron microscopy demonstrated mitochondria to be highly fragmented in DCMA fibroblasts compared to healthy control cells. Live-cell imaging demonstrated significantly increased ROS production in patient cells. These abnormalities were reversed by treating DCMA fibroblasts with SS-31, a synthetic peptide that localizes to the inner mitochondrial membrane. Levels of cardiolipin were not significantly different between control and DCMA cells and were unaffected by SS-31 treatment. Our results demonstrate the abnormal mitochondria in fibroblasts from patients with DCMA and suggest that SS-31 may represent a potential therapy for this devastating disease.

    View details for DOI 10.3389/fcvm.2019.00167

    View details for Web of Science ID 000499816700001

    View details for PubMedID 31803760

    View details for PubMedCentralID PMC6873783

  • Cellular models for human cardiomyopathy: What is the best option? WORLD JOURNAL OF CARDIOLOGY Jimenez-Tellez, N., Greenway, S. C. 2019; 11 (10): 221-235


    The genetic cardiomyopathies are a group of disorders related by abnormal myocardial structure and function. Although individually rare, these diseases collectively represent a significant health burden since they usually develop early in life and are a major cause of morbidity and mortality amongst affected children. The heterogeneity and rarity of these disorders requires the use of an appropriate model system in order to characterize the mechanism of disease and develop useful therapeutics since standard drug trials are infeasible. A common approach to study human disease involves the use of animal models, especially rodents, but due to important biological and physiological differences, this model system may not recapitulate human disease. An alternative approach for studying the metabolic cardiomyopathies relies on the use of cellular models which have most frequently been immortalized cell lines or patient-derived fibroblasts. However, the recent introduction of induced pluripotent stem cells (iPSCs), which have the ability to differentiate into any cell type in the body, is of great interest and has the potential to revolutionize the study of rare diseases. In this paper we review the advantages and disadvantages of each model system by comparing their utility for the study of mitochondrial cardiomyopathy with a particular focus on the use of iPSCs in cardiovascular biology for the modeling of rare genetic or metabolic diseases.

    View details for DOI 10.4330/wjc.v11.i10.221

    View details for Web of Science ID 000498886100002

    View details for PubMedID 31754410

    View details for PubMedCentralID PMC6859298