[en] Introduction. Mitochondrial Pyruvate Carrier (MPC) activity determines whether the pyruvate is oxidized in the mitochondria or, on the contrary, metabolized in the cytosol. It is known that, in Heart Failure (HF), a large amount of pyruvate is metabolized to lactate in the cytosol instead of following the mitochondrial pathway, so a general decrease in mitochondrial metabolism has been observed in this type of pathology. Objective. Given the relationship between mitochondrial metabolism and cardiac dysfunction, and the regulation of MPC subunit expression observed in cardiac tissues of patients with HF, the main objective of this study was to analyze the gene and protein expression of MPC1 and MPC2 molecules in blood samples, in order to study their possible use as biomarkers. Methodology. The samples used came from 4 groups of donors: patients with ischemic heart disease, idiopathic dilated cardiomyopathy or hypertrophic cardiomyopathy; and donors without cardiac pathology. Gene expression analysis was performed in whole blood samples by RT-qPCR, after the extraction of nucleic acids. The analysis of protein expression was carried out by ELISA, using plasma obtained from whole blood as a sample. Statistical analyses were performed with GraphPad Prism v8 and RCommander v4. Results. The gene expression analysis of MPC1 and MPC2 did not show statistically significant differences between the groups analyzed, except between the MH and MDI groups after removing an influential outlier from the first group. The quantification of these molecules in plasma showed undetectable results for MPC1, but in the case of MPC2, a higher protein level can be seen graphically in patients with idiopathic dilated cardiomyopathy compared to the rest of the groups. Conclusions. Our results suggest that MPC is not a Good candidate as s systemic biomarker of HF.

[gl] Introdución. A actividade da Proteína Mitocondrial Transportadora de Piruvato (MPC) determina si o piruvato se oxida nas mitocondrias ou, pola contra, se metaboliza no citosol. Sábese que, na Insuficiencia Cardíaca (IC), unha gran cantidade de piruvato é metabolizado en lactato no citosol no canto de seguir a vía mitocondrial, polo que se observou unha diminución xeral do metabolismo mitocondrial neste tipo de patoloxía. Obxectivo. Vista a relación entre o metabolismo mitocondrial e a disfunción cardíaca, e a regulación da expresión das subunidades MPC observadas nos tecidos cardíacos de pacientes con IC, o obxectivo principal deste traballo foi analizar a expresión xénica e proteica das moléculas MPC1 e MPC2 en mostras sanguíneas, para así poder estudar o seu posible uso como biomarcadores. Metodoloxía. As mostras empregadas proviñan de 4 grupos de doantes: pacientes con cardiopatía isquémica, miocardiopatía idiopática dilatada ou miocardiopatía hipertrófica; e doantes sen patoloxía cardíaca. A análise da expresión xenica realizouse en mostras de sangue total usando a técnica RT-qPCR, previa extracción dos ácidos nucleicos. A análise da expresión proteica levouse a cabo mediante a técnica ELISA, empregando como mostra o plasma obtido do sangue total. Realizáronse análises estatísticas con GraphPad Prism v8 e RCommander v4. Resultados. A análise da expresión xénica de MPC1 e MPC2 non reflectiu diferencias estatisticamente significativas entre os grupos analizados, salvoentre os grupos MH e MDI unha vez eliminado un dato atípico influente do primeiro grupo. A cuantificación destas moléculas en plasma reflectiu resultados non detectables para MPC1, pero no caso de MPC2 pódese apreciar gráficamente un maior nivel proteico en pacientes con miocardiopatía dilatada idiopática con respecto ao resto dos grupos. Conclusións. Os nosos resultados suxiren que MPC non é un bo candidato como biomarcador sistémico de IC.