Dr.-Hector-Barajas-Martinez-MMRL

Research Scientist – Molecular Genetics and Experimental Cardiology

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Area of Expertise

  • Genetic Screening and Mutation Analysis of Sudden Cardiac Death Syndromes
  • Population Genetics and Molecular Biology in disease genes markers
  • Confocal Microscopy and Gene Expression analysis by Real Time PCR
  • Molecular Physiology. Ionic distinctions among different cell types in the heart
    Molecular heterogeneity as the basis for pharmacologic distinctions in the heart
  • Biophysical and molecular mechanism for different cardiac arrhythmias like Brugada, Short QT, Long QT and Sudden Infant Death Syndromes.
  • Developmental and gender differences in cardiac electrophysiology and pharmacology.

Professional Memberships

  • Member of HUGO (Human Genome Organization)
  • Member of ABS (Biophysics Society)
  • Member of HRS (Heart Rhythm Society)
  • Member of AHA (America Heart Association) 
  • Council on Basic Cardiovascular Sciences
  • Council on Functional Genomics and Translational Biology

Research Statement

I have worked at the Masonic Medical Research Laboratory as an Associate-Professor/Research Scientist for the past 8 years. Throughout my tenure, I have been fully committed to advancing translational research in the field of genetics in cardiac arrhythmias. My role as a PD/PI investigator and team leader and Clinical Director in our Molecular Genetics Program is to establish new strategies for molecular genetic screening approaches to identified new genetic markers, prevention and treatment in inherited sudden cardiac death syndromes. I played a key role in the discovery and characterization of 8 new genes related to Brugada, Early Repolarization Syndromes and Short QT syndromes, which were published in top tier journals. 

One of the principal goals and aims is looking for new genomic medicine to decrease mortality in sudden cardiac arrhythmias.

Such as the main current proposals is to identify novel gene mutations linked to inherited cardiac arrhythmias associated with diabetes and metabolic syndromes linked with sudden cardiac death and to advance our understanding of their role in the pathophysiological phenotype at molecular and functional levels for potential personalized genomic therapies.