Moral-Sanz, J

About

After completing my Bachelor's in Pharmacy in 2007, I joined the research team of Prof. Perez-Vizcaino as an FPU fellow (Formación de Profesorado Universitario) with the objective of investigating the impact of metabolic diseases on the pulmonary vasculature, using animal models of diabetes and metabolic syndrome. My research revealed that sustained hyperglycemia had detrimental effects on the pulmonary vascular system, increasing the susceptibility to pulmonary vascular disease. This effect resembled and intensified the impact of chronic hypoxia on lung health (Lopez-Lopez et al, 2008 and 2011; Moral-Sanz et al, 2011 and 2012). These findings unveiled a clear metabolic link connecting the pulmonary pathophysiology induced by chronic hypoxia and the alterations induced by chronic hyperglycemia.

In 2013, I further pursued the exploration of this metabolic link by joining the team of Prof. A.M. Evans at the prestigious University of Edinburgh. This ambitious project, funded by the British Heart Foundation, aimed to study an essential regulator of energy balance and metabolism, the AMP-activated protein kinase (AMPK), in the context of pulmonary vascular physiology and pathophysiology. My investigations marked a significant milestone by identifying, for the first time, the mitochondria-AMPK-Kv1.5 axis and its role in the physiological response of smooth muscles to metabolic stress (Evans A.M. et al, 2015; Moral-Sanz J. et al, 2016 and 2018). Furthermore, I revealed that dysregulation of this axis precipitates cardio-pulmonary disease (Moral-Sanz et al, 2022) by promoting mitochondrial dysfunction, oxidative damage, and signs of cellular senescence in the pulmonary vascular bed.

In 2019, my growing interest in cellular senescence led me to join Dr. Ikonomopoulou's group at IMDEA Food Institute to drive a TALENTO project funded by the Madrid Community. This project focused on identifying molecular and metabolic targets of novel venom compounds with senolytic and anticancer properties. During this period, I contributed to the identification and characterization of an octopus-derived peptide with potential applications against melanoma (Moral-Sanz et al., 2021 and 2022). Additionally, I led a project aimed at discovering new senolytic compounds. The data generated in this pre-clinical project have set the proof-of-concept for new senolytic strategies, resulting in a patent and a manuscript (Moral-Sanz et al., 2025), and have attracted the attention of the Pharma and Biotech industries.

In 2024, I transitioned into industry by joining the Medical and Scientific Affairs department at Boehringer Ingelheim on behalf of Syneos Health to gain insight into clinical drug development. My current position at builds on my previous pre-clinical experience by integrating my knowledge of physiology and pharmacology, along with my attention to detail, into the communication of medical and scientific information as part of the clinical development process.

Employment

• Syneos Health Medical & Scientific Affairs
  2024 - Present
• IMDEA Food Senior Research Scientist
  2019 - 2024
• The University of Edinburgh Postdoctoral Researcher
  2013 - 2018
• Universidad Complutense de Madrid PhD Fellow
  2008 - 2012
• CIBER Enfermedades Raras Junior Researcher
  2008 - 2008
• Universidad Complutense de Madrid Predoctoral Grant (Beca de Iniciación a la Actividad Investigadora)
  2007 - 2008

Education

• Universidad Complutense de Madrid PhD
  2007 - 2012
• Universidad Complutense de Madrid Pharmacy
  2002 - 2007

Projects & Funding

Projects & funding information is unavailable.

Publications (33)

• Senotoxins target senescence via lipid binding specificity, ion imbalance and lipidome remodeling
  Nature Aging 2026 DOI: 10.1038/s43587-025-01030-w
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• Correction: The cytotoxicity of gomesin peptides is mediated by the glycosphingolipid pathway and lipid-cholesterol interactions
  Cell Death Discovery 2026 DOI: 10.1038/s41420-026-03009-x
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• The cytotoxicity of gomesin peptides is mediated by the glycosphingolipid pathway and lipid-cholesterol interactions
  Cell Death Discovery 2025 DOI: 10.1038/s41420-025-02817-x
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• AMPK deficiency in smooth muscles causes persistent pulmonary hypertension of the new-born and premature death
  Nature Communications 2022 DOI: 10.1038/s41467-022-32568-7
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• AMPK deficiency in smooth muscles causes persistent pulmonary hypertension after birth and premature death
  2022 DOI: 10.21203/rs.3.rs-424150/v1
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• The structural conformation of the tachykinin domain drives the anti-tumoural activity of an octopus peptide in melanoma BRAFV600E
  British Journal of Pharmacology 2022 DOI: 10.1111/BPH.15923
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• ERK and mTORC1 Inhibitors Enhance the Anti-Cancer Capacity of the Octpep-1 Venom-Derived Peptide in Melanoma BRAF(V600E) Mutations
  Toxins 2021 DOI: 10.3390/toxins13020146
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• Activation of K<inf>v</inf>7 channels as a novel mechanism for NO/cGMP-induced pulmonary vasodilation
  British Journal of Pharmacology 2019 DOI: 10.1111/bph.14662
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• The LKB1–AMPK-α1 signaling pathway triggers hypoxic pulmonary vasoconstriction downstream of mitochondria
  Science Signaling 2018 DOI: 10.1126/scisignal.aau0296
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• AMP-activated protein kinase inhibits K(v)1.5 channel currents of pulmonary arterial myocytes in response to hypoxia and inhibition of mitochondrial oxidative phosphorylation
  The Journal of Physiology 2016 DOI: 10.1113/JP272032
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