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Article ; Online: Circulating ST2, from biomarker to pathogenic mediator.

Pascual-Figal, Domingo / Lax, Antonio / Asensio López, María Carmen

Revista espanola de cardiologia (English ed.)

2023 Volume 76, Issue 9, Page(s) 672–674

MeSH term(s)	Humans ; Interleukin-1 Receptor-Like 1 Protein ; Biomarkers ; Heart Failure
Chemical Substances	Interleukin-1 Receptor-Like 1 Protein ; Biomarkers
Language	Spanish
Publishing date	2023-04-19
Publishing country	Spain
Document type	Journal Article
ZDB-ID	2592481-3
ISSN	1885-5857 ; 1885-5857
ISSN (online)	1885-5857
ISSN	1885-5857
DOI	10.1016/j.rec.2023.02.012
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Article: Editorial: Myocardial Remodeling: Mechanisms and Translational Implications.

Roncalli, Jerome / Tronchère, Hélène / Lax, Antonio / Kunduzova, Oxana

Frontiers in pharmacology

2022 Volume 13, Page(s) 930387

Language	English
Publishing date	2022-05-26
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2022.930387
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Article ; Online: Reply: Interleukin-1β and sST2.

Pascual-Figal, Domingo A / Lax, Antonio / Bayes-Genis, Antoni

Journal of the American College of Cardiology

2019 Volume 74, Issue 3, Page(s) 479–480

MeSH term(s)	Heart Failure ; Humans ; Inflammation ; Interleukin-1 Receptor-Like 1 Protein ; Interleukin-1beta
Chemical Substances	Interleukin-1 Receptor-Like 1 Protein ; Interleukin-1beta
Language	English
Publishing date	2019-07-18
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2019.05.021
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Zs.A 1846: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Silencing of microRNA-106b-5p prevents doxorubicin-mediated cardiotoxicity through modulation of the PR55α/YY1/sST2 signaling axis.

Lax, Antonio / Soler, Fernando / Fernandez Del Palacio, Maria Josefa / Pascual-Oliver, Silvia / Ballester, Miriam Ruiz / Fuster, Jose Javier / Pascual-Figal, Domingo / Asensio-Lopez, Maria Del Carmen

Molecular therapy. Nucleic acids

2023 Volume 32, Page(s) 704–720

Abstract: Clinical use of doxorubicin (Dox), an anthracycline with potent anti-tumor effects, is limited because of its highly chemotherapy-induced cardiotoxicity (CIC). After myocardial infarction (MI), we have recently identified Yin Yang-1 (YY1) and histone ... ...

Abstract	Clinical use of doxorubicin (Dox), an anthracycline with potent anti-tumor effects, is limited because of its highly chemotherapy-induced cardiotoxicity (CIC). After myocardial infarction (MI), we have recently identified Yin Yang-1 (YY1) and histone deacetylase 4 (HDAC4) as two factors involved in the overexpression of the isoform soluble suppression of tumorigenicity 2 (sST2) protein, which acts as a decoy receptor blocking the favorable effects of IL-33. Therefore, high levels of sST2 are associated with increased fibrosis, remodeling, and worse cardiovascular outcomes. No data exist on the role of the YY1/HDAC4/sST2 axis in CIC. This study aimed to evaluate the pathophysiological implication of the molecular YY1/HDAC4/sST2 axis in remodeling that is developed in patients treated with Dox as well as to suggest a novel molecular therapy to prevent anthracycline-induced cardiotoxicity. Here, we have characterized a novel nexus between miR106b-5p (miR-106b) levels and the YY1/HDAC4 axis in relation to the cardiac expression of
Language	English
Publishing date	2023-05-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2662631-7
ISSN	2162-2531
ISSN	2162-2531
DOI	10.1016/j.omtn.2023.04.031
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Article ; Online: The miRNA199a/SIRT1/P300/Yy1/sST2 signaling axis regulates adverse cardiac remodeling following MI.

Asensio-Lopez, Maria Carmen / Sassi, Yassine / Soler, Fernando / Fernandez Del Palacio, Maria Josefa / Pascual-Figal, Domingo / Lax, Antonio

Scientific reports

2021 Volume 11, Issue 1, Page(s) 3915

Abstract: Left ventricular remodeling following myocardial infarction (MI) is related to adverse outcome. It has been shown that an up-regulation of plasma soluble ST2 (sST2) levels are associated with lower pre-discharge left ventricular (LV) ejection fraction, ... ...

Abstract	Left ventricular remodeling following myocardial infarction (MI) is related to adverse outcome. It has been shown that an up-regulation of plasma soluble ST2 (sST2) levels are associated with lower pre-discharge left ventricular (LV) ejection fraction, adverse cardiovascular outcomes and mortality outcome after MI. The mechanisms involved in its modulation are unknown and there is not specific treatment capable of lowering plasma sST2 levels in acute-stage HF. We recently identified Yin-yang 1 (Yy1) as a transcription factor related to circulating soluble ST2 isoform (sST2) expression in infarcted myocardium. However, the underlying mechanisms involved in this process have not been thoroughly elucidated. This study aimed to evaluate the pathophysiological implication of miR-199a-5p in cardiac remodeling and the expression of the soluble ST2 isoform. Myocardial infarction (MI) was induced by permanent ligation of the left anterior coronary artery in C57BL6/J mice that randomly received antimiR199a therapy, antimiR-Ctrl or saline. A model of biomechanical stretching was also used to characterize the underlying mechanisms involved in the activation of Yy1/sST2 axis. Our results show that the significant upregulation of miR-199a-5p after myocardial infarction increases pathological cardiac hypertrophy by upregulating circulating soluble sST2 levels. AntimiR199a therapy up-regulates Sirt1 and inactivates the co-activator P300 protein, thus leading to Yy1 inhibition which decreases both expression and release of circulating sST2 by cardiomyocytes after myocardial infarction. Pharmacological inhibition of miR-199a rescues cardiac hypertrophy and heart failure in mice, offering a potential therapeutic approach for cardiac failure.
MeSH term(s)	Animals ; E1A-Associated p300 Protein/metabolism ; Hypertrophy, Left Ventricular/metabolism ; Interleukin-1 Receptor-Like 1 Protein/metabolism ; Male ; Mice, Inbred C57BL ; MicroRNAs/metabolism ; Myocardial Infarction/complications ; Myocardial Infarction/metabolism ; Myocardial Infarction/physiopathology ; Sirtuin 1/metabolism ; Ventricular Remodeling ; YY1 Transcription Factor/metabolism ; Mice
Chemical Substances	Il1rl1 protein, mouse ; Interleukin-1 Receptor-Like 1 Protein ; MicroRNAs ; Mirn199 microRNA, mouse ; YY1 Transcription Factor ; Yy1 protein, mouse ; E1A-Associated p300 Protein (EC 2.3.1.48) ; Ep300 protein, mouse (EC 2.3.1.48) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2021-02-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-82745-9
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Article ; Online: Critical warm ischemia time point for cardiac donation after circulatory death.

Sánchez-Cámara, Silvia / Asensio-López, Mari C / Royo-Villanova, Mario / Soler, Fernando / Jara-Rubio, Rubén / Garrido-Peñalver, Jose Francisco / Pinar, Eduardo / Hernández-Vicente, Álvaro / Hurtado, Jose Antonio / Lax, Antonio / Pascual-Figal, Domingo A

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons

2022 Volume 22, Issue 5, Page(s) 1321–1328

Abstract: Donation after circulatory death (DCD) represents a promising opportunity to overcome the relative shortage of donors for heart transplantation. However, the necessary period of warm ischemia is a concern. This study aims to determine the critical warm ... ...

Abstract	Donation after circulatory death (DCD) represents a promising opportunity to overcome the relative shortage of donors for heart transplantation. However, the necessary period of warm ischemia is a concern. This study aims to determine the critical warm ischemia time based on in vivo biochemical changes. Sixteen DCD non-cardiac donors, without cardiovascular disease, underwent serial endomyocardial biopsies immediately before withdrawal of life-sustaining therapy (WLST), at circulatory arrest (CA) and every 2 min thereafter. Samples were processed into representative pools to assess calcium homeostasis, mitochondrial function and cellular viability. Compared to baseline, no significant deterioration was observed in any studied parameter at the time of CA (median: 9 min; IQR: 7-13 min; range: 4-19 min). Ten min after CA, phosphorylation of cAMP-dependent protein kinase-A on Thr197 and SERCA2 decreased markedly; and parallelly, mitochondrial complex II and IV activities decreased, and caspase 3/7 activity raised significantly. These results did not differ when donors with higher WLST to CA times (≥9 min) were analyzed separately. In human cardiomyocytes, the period from WLST to CA and the first 10 min after CA were not associated with a significant compromise in cellular function or viability. These findings may help to incorporate DCD into heart transplant programs.
MeSH term(s)	Death ; Heart ; Heart Arrest ; Heart Transplantation ; Humans ; Perfusion/methods ; Tissue Donors ; Tissue and Organ Procurement ; Warm Ischemia
Language	English
Publishing date	2022-02-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2060594-8
ISSN	1600-6143 ; 1600-6135
ISSN (online)	1600-6143
ISSN	1600-6135
DOI	10.1111/ajt.16987
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Zs.A 5542: Show issues

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Article ; Online: Doxorubicin-induced oxidative stress: The protective effect of nicorandil on HL-1 cardiomyocytes.

Asensio-López, Mari C / Soler, Fernando / Pascual-Figal, Domingo / Fernández-Belda, Francisco / Lax, Antonio

PloS one

2017 Volume 12, Issue 2, Page(s) e0172803

Abstract: The primary cardiotoxic action of doxorubicin when used as antitumor drug is attributed to the generation of reactive oxygen species (ROS) therefore effective cardioprotection therapies are needed. In this sense, the antianginal drug nicorandil has been ... ...

Abstract	The primary cardiotoxic action of doxorubicin when used as antitumor drug is attributed to the generation of reactive oxygen species (ROS) therefore effective cardioprotection therapies are needed. In this sense, the antianginal drug nicorandil has been shown to be effective in cardioprotection from ischemic conditions but the underlying molecular mechanism to cope with doxorubicin-induced ROS is unclear. Our in vitro study using the HL-1 cardiomyocyte cell line derived from mouse atria reveals that the endogenous nitric oxide (NO) production was stimulated by nicorandil and arrested by NO synthase inhibition. Moreover, while the NO synthase activity was inhibited by doxorubicin-induced ROS, the NO synthase inhibition did not affect doxorubicin-induced ROS. The inhibition of NO synthase activity by doxorubicin was totally prevented by preincubation with nicorandil. Nicorandil also concentration-dependently (10 to 100 μM) decreased doxorubicin-induced ROS and the effect was antagonized by 5-hydroxydecanoate. The inhibition profile of doxorubicin-induced ROS by nicorandil was unaltered when an L-arginine derivative or a protein kinase G inhibitor was present. Preincubation with pinacidil mimicked the effect of nicorandil and the protection was eliminated by glibenclamide. Quantitative colocalization of fluorescence indicated that the mitochondrion was the target organelle of nicorandil and the observed response was a decrease in the mitochondrial inner membrane potential. Interference with H+ movement across the mitochondrial inner membrane, leading to depolarization, also protected from doxorubicin-induced ROS. The data indicate that activation of the mitochondrial ATP-sensitive K+ channel by nicorandil causing mitochondrial depolarization, without participation of the NO donor activity, was responsible for inhibition of the mitochondrial NADPH oxidase that is the main contributor to ROS production in cardiomyocytes. Impairment of the cytosolic Ca2+ signal induced by caffeine and the increase in lipid peroxidation, both of which are indicators of doxorubicin-induced oxidative stress, were also prevented by nicorandil.
MeSH term(s)	Animals ; Calcium/metabolism ; Cell Line ; Doxorubicin/pharmacology ; Lipid Peroxidation/drug effects ; Mice ; Mitochondria/drug effects ; Mitochondria/metabolism ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Nicorandil/pharmacology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/metabolism ; Oxidative Stress/drug effects ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species ; Nicorandil (260456HAM0) ; Nitric Oxide (31C4KY9ESH) ; Doxorubicin (80168379AG) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2017-02-28
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0172803
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Article ; Online: Pharmacological inhibition of the mitochondrial NADPH oxidase 4/PKCα/Gal-3 pathway reduces left ventricular fibrosis following myocardial infarction.

Asensio-Lopez, Maria Del Carmen / Lax, Antonio / Fernandez Del Palacio, Maria Josefa / Sassi, Yassine / Hajjar, Roger J / Pascual-Figal, Domingo A

Translational research : the journal of laboratory and clinical medicine

2018 Volume 199, Page(s) 4–23

Abstract: Although the initial reparative fibrosis after myocardial infarction (MI) is crucial for preventing rupture of the ventricular wall, an exaggerated fibrotic response and reactive fibrosis outside the injured area are detrimental. Although metformin ... ...

Abstract	Although the initial reparative fibrosis after myocardial infarction (MI) is crucial for preventing rupture of the ventricular wall, an exaggerated fibrotic response and reactive fibrosis outside the injured area are detrimental. Although metformin prevents adverse cardiac remodeling, as well as provides glycemic control, the underlying mechanisms remain poorly documented. This study describes the effect of mitochondrial NADPH oxidase 4 (mitoNox) and protein kinase C-alpha (PKCα) on the cardiac fibrosis and galectin 3 (Gal-3) expression. Randomly rats underwent MI, received metformin or saline solution. A model of biomechanical strain and co-culturewas used to enable cross talk between cardiomyocytes and fibroblasts. Long-term metformin treatment after MIwas associated with (1) a reduction in myocardial fibrosis and Gal-3 levels; (2) an increase in adenosine monophosphate-activated protein kinase (AMPK) α1/α2 levels; and (3) an inhibition of both mRNA expression and enzymatic activities of mitoNox and PKCα. These findings were replicated in the cellular model, where the silencing of AMPK expression blocked the ability of metformin to protect cardiomyocytes from strain. The use of specific inhibitors or small interference RNA provided evidence that PKCα is downstream of mitoNox, and that the activation of this pathway results in Gal-3 upregulation.The Gal-3 secreted by cardiomyocytes has a paracrine effect on cardiac fibroblasts, inducing their activation. In conclusion, a metformin-induced increase in AMPK improves myocardial remodeling post-MI, which is related to the inhibition of the mitoNox/PKCα/Gal-3 pathway. Manipulation of this pathway might offer new therapeutic options against adverse cardiac remodeling, in terms of preventing the activation of the present fibroblast population.
MeSH term(s)	Adenylate Kinase/biosynthesis ; Animals ; Cells, Cultured ; Culture Media, Conditioned ; Enzyme Induction ; Fibrosis/prevention & control ; Galectin 3/antagonists & inhibitors ; Heart Ventricles/pathology ; Male ; Metformin/pharmacology ; Mice ; Mitochondria, Heart/drug effects ; Mitochondria, Heart/enzymology ; Myocardial Infarction/complications ; Myocardial Infarction/pathology ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/metabolism ; NADPH Oxidases/antagonists & inhibitors ; Protein Kinase C-alpha/antagonists & inhibitors ; Rats, Sprague-Dawley ; Signal Transduction/drug effects ; Ventricular Remodeling/drug effects
Chemical Substances	Culture Media, Conditioned ; Galectin 3 ; Metformin (9100L32L2N) ; NADPH Oxidases (EC 1.6.3.-) ; Protein Kinase C-alpha (EC 2.7.11.13) ; Adenylate Kinase (EC 2.7.4.3)
Language	English
Publishing date	2018-04-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2246684-8
ISSN	1878-1810 ; 1532-6543 ; 1931-5244
ISSN (online)	1878-1810 ; 1532-6543
ISSN	1931-5244
DOI	10.1016/j.trsl.2018.04.004
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Article ; Online: Empagliflozin improves post-infarction cardiac remodeling through GTP enzyme cyclohydrolase 1 and irrespective of diabetes status.

Asensio Lopez, Maria Del Carmen / Lax, Antonio / Hernandez Vicente, Alvaro / Saura Guillen, Elena / Hernandez-Martinez, Antonio / Fernandez Del Palacio, Maria Josefa / Bayes-Genis, Antoni / Pascual Figal, Domingo A

Scientific reports

2020 Volume 10, Issue 1, Page(s) 13553

Abstract: Sodium-glucose co-transporter-2 inhibitors (SGLT2i) have shown to prevent heart failure progression, although the mechanisms remain poorly understood. Here we evaluated the effect of empagliflozin (EMPA, SGLT2i) in cardiac remodeling after myocardial ... ...

Abstract	Sodium-glucose co-transporter-2 inhibitors (SGLT2i) have shown to prevent heart failure progression, although the mechanisms remain poorly understood. Here we evaluated the effect of empagliflozin (EMPA, SGLT2i) in cardiac remodeling after myocardial infarction, the interplay with diabetes status and the role of cardiac GTP enzyme cyclohydrolase 1 (cGCH1). A rat model of diabetes (50 mg/kg streptozotocin, i.p.) was subjected to myocardial infarction and left ventricular systolic dysfunction, by ligation of the left anterior descending coronary artery. EMPA therapy significantly improved cardiac remodeling parameters and ameliorated processes of fibrosis and hypertrophy, in both non-diabetic and diabetic rats. This cardioprotective effect related with a significant increase in myocardial expression levels of cGCH1, which led to activation of nNOS and eNOS, and inhibition of iNOS, and subsequently resulted in increasing of NO levels and decreasing O
MeSH term(s)	Animals ; Benzhydryl Compounds/pharmacology ; Diabetes Mellitus, Experimental/physiopathology ; GTP Cyclohydrolase/genetics ; GTP Cyclohydrolase/metabolism ; Glucosides/pharmacology ; Male ; Myocardial Infarction/complications ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Rats ; Rats, Wistar ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Ventricular Dysfunction, Left/drug therapy ; Ventricular Dysfunction, Left/etiology ; Ventricular Dysfunction, Left/metabolism ; Ventricular Dysfunction, Left/pathology ; Ventricular Remodeling/drug effects
Chemical Substances	Benzhydryl Compounds ; Glucosides ; Sodium-Glucose Transporter 2 Inhibitors ; GTP Cyclohydrolase (EC 3.5.4.16) ; Gch1 protein, rat (EC 3.5.4.16) ; empagliflozin (HDC1R2M35U)
Language	English
Publishing date	2020-08-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-70454-8
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Article ; Online: Author Correction: Empagliflozin improves post-infarction cardiac remodeling through GTP enzyme cyclohydrolase 1 and irrespective of diabetes status.

Del Carmen Asensio Lopez, Maria / Lax, Antonio / Hernandez Vicente, Alvaro / Saura Guillen, Elena / Hernandez-Martinez, Antonio / Fernandez Del Palacio, Maria Josefa / Bayes-Genis, Antoni / Pascual Figal, Domingo A

Scientific reports

2020 Volume 10, Issue 1, Page(s) 17266

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

Abstract	An amendment to this paper has been published and can be accessed via a link at the top of the paper.
Language	English
Publishing date	2020-10-09
Publishing country	England
Document type	Published Erratum
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-73065-5
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