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I have been worked, since the beginning of my career, in design novel therapeutic strategies based on mechanistic knowledge to prevent remodeling and cardiac dysfunction, which develop in patients who have suffered myocardial infarction (MI) or are receiving chemotherapy. After completing a BSc in Biochemistry [University of Murcia (UM)], I joined the Pascual-Figal´s Lab (IMIB&UM) supported with competitive funds. In detail, my findings on the mechanisms underlying cardiac remodeling, and in focus on IL33/ST2 system, are an international benchmark. The know-how in computational genomics and training in animal models, acquired during my stay at the Hajjar´s Lab (USA), were essential: (i) To achieve specific aims of the projects which funded this line with international groups [Hajjar (USA); Sassi´s lab (USA)]; and (ii) To lead the design of the first therapy able to decrease sST2 protein, a poor prognostic marker in heart failure (HF). My work allowed characterized the sST2 transcription by Yin yang-1 (YY1) and defined the regulatory mechanism. Accordingly, I hypothesized that silencing of YY1 might lowering sST2 levels, which may stand for a new therapeutic paradigm. My expertise, in collaboration with Sassi´s team (USA), allowed me: (i) To design an RNAi aimed at blocking the expression of YY1 (named BC13); and (ii) To demonstrate its effectiveness to prevent remodeling and cardiac dysfunction after MI. Note that BC-13 is the first therapy able to specifically lower sST2 to improve the evolution of patients that have suffered a MI. These results have been patented, published, were shown as highlights (HF Congress -2015, -18), accepted in the HFA Meeting 2015, -18, -19, -23 and 2nd prize best oral communication (SEC2021 Congress). Currently, BC13 is in the preclinical phase to determine its safety. Moreover, investigating the nature of the connection between higher sST2 levels and cancer treatment-induced cardiotoxicity (CIC), represents another important line of research in my career. Note that, existing therapies for CIC are suboptimal and initiated too late. The acquired skills during my training [Pascual-Figal´s lab (IMIB&UM)], with input from Lax´s team (IMIB&UM) in animal models and Sassi´s team (USA) in gene therapy, allowed me hypothesized that myocardium could acted as a source of sST2 during chemo which could be related to CIC. Leading specific experimental aims, I´ve headed of the experimental lab, designing and carrying out the assays and developing the experimental models. One of the key findings is the confirmation of my hypothesis reported the cardiac expression of sST2 and its relationship with CIC. Mechanistically, I also contributed to identify microRNA106b as key target and designing an antimiR106b (AM106) as therapy, lowering sST2 levels and improving cardiac function in mice. The results provide the basis for proposing sST2 as a novel poor prognostic marker in CIC and AM106 as therapeutic. In addition, I´ve obtained a project as co-leader, where Sassi (USA) is assessor. In parallel, my know-how in contractility, with input from Pascual-Figal´s team (IMIB&UM), allowed me to lead the aims of a project, which has been a turning point in the field of transplantation. My work has allowed to incorporate donations after circulatory death (DCD) into transplant programs. I was able to identify the time-window in which the myocardium was able to maintain its contractile capacity after DCD. Data which allowed me obtained a PhD with honors. Moreover, my training has allowed me to establish a murine heart transplantation model, become a beneficiary of a JdC-grant (CNIC), and obtained a project as co-leader. Here, I´m evaluating the effects of clonal hematopoiesis, focus on Tet2-/-, in the development of cardiac dysfunction. This project is improving my technical-scientific skills and the results will be translated into the national system as a new therapeutic approach for HF in the framework of personalized medicine. In parallel, my know-how has been exploited in the pursuit of three R&D projects with international companies: (i) Novartis, Characterization of serelaxin administration effects; (ii) ELPozo, To development of the range of meat products BienStar; and (iii) Genentech, Impact of anti-ST2 therapy in cardiac remodeling. In addition, BioCardio SL, is exploiting my patented results. My research work consists of over 29 original articles. It has obtained >920 citations [Google Scholar; h-index of 14]. Moreover, I´ve: (i) Executed an ad-hoc communication and dissemination plan acting in >90 congress as presenter, webpage, twitter account,··; (ii) Participated in >14 projects and co-PL in 1; (iii) Start-up founder. Technology Based Company [BioCardio S.L.]; and (iv) Directed the extracurricular internships for 2 students, 2 undergraduate thesis projects, and 2 PhD students. At present, I´m editor of 2 prestigious journals [IJMC; Front Pharmacol].
Research Interests
Papers共 58 篇Author StatisticsCo-AuthorSimilar Experts
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A. Antonio Manuel Lax, M. Ruiz-Ballester, S. Pascual-Oliver,A. Hernandez-Vicente,F. Soler,M. J. Fernandez Del Palacio,D. A. Pascual-Figal,M. C. Asensio-Lopez
EUROPEAN JOURNAL OF HEART FAILURE (2023): 20-20
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A. Alvaro Hernandez-Vicente,C. Marti-Gomez,D. Saura-Espin,M. J. Oliva-Sandoval,F. Pastor-Perez, A. Riquelme-Perez, C. Sanchez-Perez,M. C. Asensio-Lopez,M. D. Espinosa,M. Gomez-Molina,C. Caro, J. M. Vivo-Molina,
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semanticscholar(2020)
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J. Sánchez-Más, E. Saura-Guillén,M.C. Asensio-López, Á. Soriano-Filiu, M. Carmen Sánchez-Pérez, A.M. Hernandez-Martinez,A. Lax,D. Pascual-Figal
Diabetes & Metabolismno. 2 (2019): 201-204
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Author Statistics
#Papers: 61
#Citation: 888
H-Index: 16
G-Index: 29
Sociability: 5
Diversity: 0
Activity: 0
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