Publicaciones

Induction of RISK by HMG-CoA reductase inhibition affords cardioprotection after myocardial infarction

Gemma Vilahur, Laura Casaní, Esther Pena, Xavier Duran, Oriol Juan-Babot, Lina Badimon. Induction of RISK by HMG-CoA reductase inhibition affords cardioprotection after myocardial infarction. Atherosclerosis 206 (2009) 95–101. Conclusions: HMG-CoA inhibition early after reperfusion activates RISK kinases, reduces the extent of damaged myocardium, and improves heart function.

Molecular and cellular mechanisms involved in cardiac remodeling after acute myocardial infarction

Gemma Vilahur, Oriol Juan-Babot, Esther Peña, Blanca Oñate, Laura Casaní, Lina Badimon. Molecular and cellular mechanisms involved in cardiac remodeling after acute myocardial infarction. Journal of Molecular and Cellular Cardiology 50 (2011) 522–533. Results and Conclusions: Accordingly, leukocytes and macrophages are progressively recruited to the IM (P≤0.05). Ischemia up-regulates pro-fibrotic TGF-β that gradually rises collagen1-A1/-A3 mRNA with subsequent increase in total collagen fibrils and fibroblasts from 3 days-R onwards (P≤0.005). MMP-2 activity increases from ischemia to 3 days post-R (P≤0.05). We report that there is a timely coordinated cellular and molecular response to myocardial ischemia and R within the first 6 days after MI. In-depth understanding of the mechanisms involved in tissue repair is warranted to timely intervene and better define novel cardioprotective strategies.

HMG-CoA reductase inhibition prior reperfusion improves reparative fibrosis post-myocardial infarction in a preclinical experimental model

Gemma Vilahur, Laura Casaní, Esther Peña, Oriol Juan-Babot, Guiomar Mendieta, Javier Crespo, Lina Badimon. HMG-CoA reductase inhibition prior reperfusion improves reparative fibrosis post-myocardial infarction in a preclinical experimental model. International Journal of Cardiology 175 (2014) 528–538. Conclusions: Acute HMG-CoA-reductase inhibition during total ischemia and prior reperfusion limits reperfusion injury and prolonged oral simvastatin treatment thereafter improves cardiac healing post-MI.

 

Network-Assisted Systems Biology Analysis of the Mitochondrial Proteome in a Pre-Clinical Model of Ischemia, Revascularization and Post-Conditioning

Alex Gallinat, Gemma Vilahur, Teresa Padró and Lina Badimon. Network-Assisted Systems Biology Analysis of the Mitochondrial Proteome in a Pre-Clinical Model of Ischemia, Revascularization and Post-Conditioning. Int. J. Mol. Sci. 2022, 23, 2087. https://doi.org/ 10.3390/ijms23042087. Collectively, our results identify cardiac metabolism as a driver of cardioprotection, highlighting a dual role for post-conditioning promoting metabolic reprogramming of the myocardium, and a protective response mediated by VDAC2 and DJ-1 in the mitochondria.

A Novel ELISA for the Quantification of Serum Levels of 2 Glycosylated Variants of Apolipoprotein J: Biomarkers for Myocardial Ischemia

Lola Fernández Encinas, Nuria Lluch, Alan H B Wu, Juan Carlos Kaski, Lina Badimon, Judit Cubedo, A Novel ELISA for the Quantification of Serum Levels of 2 Glycosylated Variants of Apolipoprotein J: Biomarkers for Myocardial Ischemia, The Journal of Applied Laboratory Medicine, Volume 8, Issue 5, September 2023, Pages 917–930, Conclusions: The newly developed ELISAs to quantify ApoJ-GlycA2 and ApoJ-GlycA6 serum levels showed an acceptable analytical performance according to European Medicines Agency guidelines on bioanalytical method validation in terms of precision, accuracy, recovery, cross-reactivity, and stability.

Infiltrated cardiac lipids impair myofibroblast-induced healing of the myocardial scar post-myocardial infarction

Gemma Vilahur, Laura Casaní, Oriol Juan-Babot, José M. Guerra, Lina Badimon. Infiltrated cardiac lipids impair myofibroblast-induced healing of the myocardial scar post-myocardial infarction. Atherosclerosis 224 (2012) 368-376. Conclusion: Intramyocardial lipid accumulation impairs TGFb/TbRII/Smad2/3 signaling altering the fibrotic reparative process of the scar resulting in larger infarcts and cardiac dysfunction.

Reperfusion-triggered stress protein response in the myocardium is blocked by post-conditioning. Systems biology pathway analysis highlights the key role of the canonical aryl-hydrocarbon receptor pathway

Gemma Vilahur, Judit Cubedo, Laura Casaní, Teresa Padró, Manel Sabaté-Tenas, Juan J. Badimon, and Lina Badimon. Reperfusion-triggered stress protein response in the myocardium is blocked by post-conditioning. Systems biology pathway analysis highlights the key role of the canonical aryl-hydrocarbon receptor pathway. European Heart Journal (2013) 34, 2082–2093. Conclusion: Ischaemic post-conditioning improves cardiac function post-myocardial infarction and reduces reperfusion-induced cell damage by down-regulation of the AhR-signalling transduction pathway ultimately leading to infarct size reduction.

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