María Monsalve graduated in Biology at the “Universidad Autónoma de Madrid” (UAM), and was awarded a PhD degree in Biochemistry and Molecular Biology at UAM. Currently, she holds a tenure position, “Científico Titular” (CSIC), at the “Instituto de Investigaciones Biomédicas Alberto Sols” (IIBm, CSIC-UAM) in Madrid (Spain) where she is a Research Group Leader.
María Monsalve is Vice-president of the “Grupo Español de Investigación en Radicales Libres” (GEIRLI), Coordinator of the “Grupo de Estrés Oxidativo de la Sociedad Española de Bioqúimica y Biología Molecular” (SEBBM). María Monsalve is also Council Member of the European Society for Free Radical Research (SFRR-europe) and Management Committee Member of the European COST action CA15203-Mitoeagle.
As a group leader her main research interest is to understand the role played by the control of mitochondrial activity, in particular control of mitochondrial oxidative stress in human metabolic diseases, including type 2 diabetes. She has been awarded 2 regional, 8 national and 1 european competitive grants as Principal Investigator and she has supervised 5 PhD Thesis and 3 Master Thesis.
Currently, her research focuses on the identification of non invasive markers of metabolic dysregulation that can be used for personalized medicine approaches and patient stratification.
1. TREATMENT project
ESR3 will evaluate Drug-induced mitochondrial dysfunction to unravel how antipsychotic drug catabolism in the liver alters mitochondrial activity, and how the ensuing modified activity of master transcriptional regulators controlling oxidative metabolism may led to general metabolic dysfunctions including fibrosis. The ESR will study drug specific differences on mitochondrial activity, as well as different capacity of the model animals to cope with the alterations in mitochondrial activity. The ESR will analyse background and drug specific differences in the induction of mitochondrial biogenesis (PGC1α/β, TFAM, SIRT3) as a compensatory response of the liver to mitochondrial dysfunction and in the capacity to fully recover mitochondrial function that if limited, would result in the accumulation of dysfunctional mitochondria and elevated ROS. The final aim of the study would be to determine how these limitations in the mitochondrial oxidative capacity contribute to long term metabolic dysfunctions following chronic drug administration.
ESR4 will analyze the role of mitochondrial dysfunction in drug-induced cardiovascular disease in order to evaluate to what extent drug induced mitochondrial dysfunction may result in the development of cardiovascular disease. The ESR will evaluate the genetic basis for variability on drug induced mitochondrial dysfunction on cardiovascular disease. Mitochondrial dysfunction is associated with cardiovascular disease, hence the putative impact of drug induced mitochondrial dysfunction on the cardiovascular system will be studied analyzing both macrovascular and microvascular complications. To that end the ESR will test the effects of psychotropic drugs on endothelial dysfunction, atheroma plaque formation, angiogenesis and retinopathy.
2. Some Recent Publications
- PGC-1α downregulation in the steatotic liver enhances ischemia-reperfusion injury and impairs ischemic preconditioning.
Sánchez Ramos C, Prieto I, Tierrez A, Laso J, Valdecantos MP, Bartrons R, Rosello-Catafau J, Monsalve M.
Antioxid Redox Signal. 2017 Mar 7. doi: 10.1089/ars.2016.6836. [Epub ahead of print]
- Heme-Oxygenase I and PCG-1α Regulate Mitochondrial Biogenesis via Microglial Activation of Alpha7 Nicotinic Acetylcholine Receptors Using PNU282987.
Navarro E, Gonzalez-Lafuente L, Pérez-Liébana I, Buendia I, López-Bernardo E, Sánchez-Ramos C, Prieto I, Cuadrado A, Satrustegui J, Cadenas S, Monsalve M, López MG.
Antioxid Redox Signal. 2016 Sep 30. [Epub ahead of print]
- Oxidative stress induces loss of pericyte coverage and vascular instability in PGC-1α-deficient mice.
García-Quintans N, Sánchez-Ramos C, Prieto I, Tierrez A, Arza E, Alfranca A, Redondo JM, Monsalve M.
Angiogenesis. 2016 Apr;19(2):217-28. doi: 10.1007/s10456-016-9502-0. Epub 2016 Mar 7.
- Regulation of endothelial dynamics by PGC-1α relies on ROS control of VEGF-A signaling.
García-Quintans N, Prieto I, Sánchez-Ramos C, Luque A, Arza E, Olmos Y, Monsalve M.
Free Radic Biol Med. 2016 Apr;93:41-51. doi: 10.1016/j.freeradbiomed.2016.01.021. Epub 2016 Jan 29.
For a full publication record, go to Orcid, Code 0000-0003-2796-1453