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  1. Article: Inhibition of NOX2 or NLRP3 inflammasome prevents cardiac remote ischemic preconditioning.

    Benavides, Sandra / Palavecino, Rodrigo / Riquelme, Jaime A / Montecinos, Luis / Finkelstein, José Pablo / Donoso, Paulina / Sánchez, Gina

    Frontiers in physiology

    2024  Volume 14, Page(s) 1327402

    Abstract: Introduction: ...

    Abstract Introduction:
    Language English
    Publishing date 2024-01-15
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2023.1327402
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Novel Strategies to Improve the Cardioprotective Effects of Cardioplegia.

    Osorio-Llanes, Estefanie / Castellar-López, Jairo / Rosales-Rada, Wendy / Montoya, Yulieth / Bustamante, John / Zalaquett, Ricardo / Bravo-Sagua, Roberto / Riquelme, Jaime A / Sánchez, Gina / Chiong, Mario / Lavandero, Sergio / Mendoza-Torres, Evelyn

    Current cardiology reviews

    2024  

    Abstract: The use of cardioprotective strategies as adjuvants of cardioplegic solutions has become an ideal alternative for the improvement of post-surgery heart recovery. The choice of the optimal cardioplegia, as well as its distribution mechanism, remains ... ...

    Abstract The use of cardioprotective strategies as adjuvants of cardioplegic solutions has become an ideal alternative for the improvement of post-surgery heart recovery. The choice of the optimal cardioplegia, as well as its distribution mechanism, remains controversial in the field of cardiovascular surgery. There is still a need to search for new and better cardioprotective methods during cardioplegic procedures. New techniques for the management of cardiovascular complications during cardioplegia have evolved with new alternatives and additives, and each new strategy provides a tool to neutralize the damage after ischemia/reperfusion events. Researchers and clinicians have committed themselves to studying the effect of new strategies and adjuvant components with the potential to improve the cardioprotective effect of cardioplegic solutions in preventing myocardial ischemia/reperfusion-induced injury during cardiac surgery. The aim of this review is to explore the different types of cardioplegia, their protection mechanisms, and which strategies have been proposed to enhance the function of these solutions in hearts exposed to cardiovascular pathologies that require surgical alternatives for their corrective progression.
    Language English
    Publishing date 2024-01-24
    Publishing country United Arab Emirates
    Document type Journal Article
    ISSN 1875-6557
    ISSN (online) 1875-6557
    DOI 10.2174/011573403X263956231129064455
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Targeting the Endothelium to Achieve Cardioprotection.

    Herrera-Zelada, Nicolas / Zuñiga-Cuevas, Ursula / Ramirez-Reyes, Andres / Lavandero, Sergio / Riquelme, Jaime A

    Frontiers in pharmacology

    2021  Volume 12, Page(s) 636134

    Abstract: Despite considerable improvements in the treatment of myocardial infarction, it is still a highly prevalent disease worldwide. Novel therapeutic strategies to limit infarct size are required to protect myocardial function and thus, avoid heart failure ... ...

    Abstract Despite considerable improvements in the treatment of myocardial infarction, it is still a highly prevalent disease worldwide. Novel therapeutic strategies to limit infarct size are required to protect myocardial function and thus, avoid heart failure progression. Cardioprotection is a research topic with significant achievements in the context of basic science. However, translation of the beneficial effects of protective approaches from bench to bedside has proven difficult. Therefore, there is still an unmet need to study new avenues leading to protecting the myocardium against infarction. In line with this, the endothelium is an essential component of the cardiovascular system with multiple therapeutic targets with cardioprotective potential. Endothelial cells are the most abundant non-myocyte cell type in the heart and are key players in cardiovascular physiology and pathophysiology. These cells can regulate vascular tone, angiogenesis, hemostasis, and inflammation. Accordingly, endothelial dysfunction plays a fundamental role in cardiovascular diseases, which may ultimately lead to myocardial infarction. The endothelium is of paramount importance to protect the myocardium from ischemia/reperfusion injury via conditioning strategies or cardioprotective drugs. This review will provide updated information on the most promising therapeutic agents and protective approaches targeting endothelial cells in the context of myocardial infarction.
    Language English
    Publishing date 2021-02-02
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2021.636134
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Heart Disease and Cancer: Are the Two Killers Colluding?

    Kitsis, Richard N / Riquelme, Jaime A / Lavandero, Sergio

    Circulation

    2018  Volume 138, Issue 7, Page(s) 692–695

    MeSH term(s) Heart Diseases ; Heart Failure ; Heart Transplantation ; Humans ; Neoplasms
    Language English
    Publishing date 2018-10-24
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.118.033907
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui IV Zs.60: Show issues Location:
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  5. Article ; Online: Editorial commentary: Cardiometabolic diseases and gut microbiota-removing the veil.

    Riquelme, Jaime A / Ferreccio, Catterina / Lavandero, Sergio

    Trends in cardiovascular medicine

    2018  Volume 29, Issue 3, Page(s) 148–149

    MeSH term(s) Cardiovascular Diseases ; Gastrointestinal Microbiome ; Humans
    Language English
    Publishing date 2018-09-04
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 1097434-9
    ISSN 1873-2615 ; 1050-1738
    ISSN (online) 1873-2615
    ISSN 1050-1738
    DOI 10.1016/j.tcm.2018.08.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3419: Show issues Location:
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  6. Article: The aging of ER-mitochondria communication: A journey from undifferentiated to aged cells.

    Morgado-Cáceres, Pablo / Liabeuf, Gianella / Calle, Ximena / Briones, Lautaro / Riquelme, Jaime A / Bravo-Sagua, Roberto / Parra, Valentina

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 946678

    Abstract: The complex physiology of eukaryotic cells requires that a variety of subcellular organelles perform unique tasks, even though they form highly dynamic communication networks. In the case of the endoplasmic reticulum (ER) and mitochondria, their ... ...

    Abstract The complex physiology of eukaryotic cells requires that a variety of subcellular organelles perform unique tasks, even though they form highly dynamic communication networks. In the case of the endoplasmic reticulum (ER) and mitochondria, their functional coupling relies on the physical interaction between their membranes, mediated by domains known as mitochondria-ER contacts (MERCs). MERCs act as shuttles for calcium and lipid transfer between organelles, and for the nucleation of other subcellular processes. Of note, mounting evidence shows that they are heterogeneous structures, which display divergent behaviors depending on the cell type. Furthermore, MERCs are plastic structures that remodel according to intra- and extracellular cues, thereby adjusting the function of both organelles to the cellular needs. In consonance with this notion, the malfunction of MERCs reportedly contributes to the development of several age-related disorders. Here, we integrate current literature to describe how MERCs change, starting from undifferentiated cells, and their transit through specialization, malignant transformation (i.e., dedifferentiation), and aging/senescence. Along this journey, we will review the function of MERCs and their relevance for pivotal cell types, such as stem and cancer cells, cardiac, skeletal, and smooth myocytes, neurons, leukocytes, and hepatocytes, which intervene in the progression of chronic diseases related to age.
    Language English
    Publishing date 2022-08-19
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.946678
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Regulation of total LC3 levels by angiotensin II in vascular smooth muscle cells.

    Mondaca-Ruff, David / Quiroga, Clara / Norambuena-Soto, Ignacio / Riquelme, Jaime A / San Martin, Alejandra / Bustamante, Mario / Lavandero, Sergio / Chiong, Mario

    Journal of cellular and molecular medicine

    2022  Volume 26, Issue 5, Page(s) 1710–1713

    Abstract: Hypertension is associated with high circulating angiotensin II (Ang II). We have reported that autophagy regulates Ang II-induced vascular smooth muscle cell (VSMC) hypertrophy, but the mechanism mediating this effect is still unknown. Therefore, we ... ...

    Abstract Hypertension is associated with high circulating angiotensin II (Ang II). We have reported that autophagy regulates Ang II-induced vascular smooth muscle cell (VSMC) hypertrophy, but the mechanism mediating this effect is still unknown. Therefore, we studied how Ang II regulates LC3 levels in VSMCs and whether Bag3, a co-chaperone known to regulate LC3 total levels, may be involved in the effects elicited by Ang II. A7r5 cell line or rat aortic smooth muscle cell (RASMC) primary culture were stimulated with Ang II 100 nM for 24 h and LC3 I, LC3 II and Bag3 protein levels were determined by Western blot. MAP1LC3B mRNA levels were assessed by RT-qPCR. Ang II increased MAP1LC3B mRNA levels and protein levels of LC3 I, LC3 II and total LC3 (LC3 I + LC3 II). Cycloheximide, but not actinomycin D, abolished LC3 II and total LC3 increase elicited by Ang II in RASMCs. In A7r5 cells, cycloheximide prevented the Ang II-mediated increase of LC3 I and total LC3, but not LC3 II. Moreover, Ang II increased Bag3 levels, but this increase was not observed upon co-administration with either losartan 1 μM (AT1R antagonist) or Y-27632 10 μM (ROCK inhibitor). These results suggest that Ang II may regulate total LC3 content through transcriptional and translational mechanisms. Moreover, Bag3 is increased in response to Ang II by a AT1R/ROCK signalling pathway. These data provide preliminary evidence suggesting that Ang II may stimulate autophagy in VSMCs by increasing total LC3 content and LC3 processing.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Angiotensin II/metabolism ; Angiotensin II/pharmacology ; Animals ; Apoptosis Regulatory Proteins/metabolism ; Cells, Cultured ; Cycloheximide/metabolism ; Cycloheximide/pharmacology ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/metabolism ; RNA, Messenger/genetics ; Rats
    Chemical Substances Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; BAG3 protein, rat ; LC3 protein, rat ; Microtubule-Associated Proteins ; RNA, Messenger ; Angiotensin II (11128-99-7) ; Cycloheximide (98600C0908)
    Language English
    Publishing date 2022-02-03
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.17215
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5752: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  8. Article: Endothelial activation impairs the function of small extracellular vesicles.

    Herrera-Zelada, Nicolas / Zúñiga-Cuevas, Úrsula / Ramírez-Reyes, Andrés / Norambuena-Soto, Ignacio / Venegas-Zamora, Leslye / Troncoso, Mayarling F / Hernández, Alejandra / Sánchez, Gina / Pedrozo, Zully / Lavandero, Sergio / Riquelme, Jaime A

    Frontiers in pharmacology

    2023  Volume 14, Page(s) 1143888

    Abstract: Small extracellular vesicles are nanosized vesicles (30-200 nm) that can ferry proteins, nucleic acids, and lipids between cells and therefore, have significant potential as biomarkers, drug delivery tools or therapeutic agents. SEVs of endothelial ... ...

    Abstract Small extracellular vesicles are nanosized vesicles (30-200 nm) that can ferry proteins, nucleic acids, and lipids between cells and therefore, have significant potential as biomarkers, drug delivery tools or therapeutic agents. SEVs of endothelial origin have been shown to -among other functions-reduce
    Language English
    Publishing date 2023-03-27
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2023.1143888
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  9. Article: Methods for studying primary cilia in heart tissue after ischemia-reperfusion injury.

    Kretschmar, Catalina / Hernández-Cáceres, María Paz / Reyes, Montserrat / Peña-Oyarzún, Daniel / García-Navarrete, Camila / Troncoso, Rodrigo / Díaz-Castro, Francisco / Budini, Mauricio / Morselli, Eugenia / Riquelme, Jaime A / Hill, Joseph A / Lavandero, Sergio / Criollo, Alfredo

    Methods in cell biology

    2023  Volume 176, Page(s) 85–101

    Abstract: Cardiovascular diseases are the leading cause of death and disability worldwide. After heart injury triggered by myocardial ischemia or myocardial infarction, extensive zones of tissue are damaged and some of the tissue dies by necrosis and/or apoptosis. ...

    Abstract Cardiovascular diseases are the leading cause of death and disability worldwide. After heart injury triggered by myocardial ischemia or myocardial infarction, extensive zones of tissue are damaged and some of the tissue dies by necrosis and/or apoptosis. The loss of contractile mass activates a series of biochemical mechanisms that allow, through cardiac remodeling, the replacement of the dysfunctional heart tissue by fibrotic material. Our previous studies have shown that primary cilia, non-motile antenna-like structures at the cell surface required for the activation of specific signaling pathways, are present in cardiac fibroblasts and required for cardiac fibrosis induced by ischemia/reperfusion (I/R) in mice. I/R-induced myocardial fibrosis promotes the enrichment of ciliated cardiac fibroblasts where the myocardial injury occurs. Given discussions about the existence of cilia in specific cardiac cell types, as well as the functional relevance of studying cilia-dependent signaling in cardiac fibrosis after I/R, here we describe our methods to evaluate the presence and roles of primary cilia in cardiac fibrosis after I/R in mice.
    MeSH term(s) Mice ; Animals ; Cilia/metabolism ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/pathology ; Heart ; Myocardial Infarction ; Fibrosis ; Myocytes, Cardiac/metabolism ; Myocardium
    Language English
    Publishing date 2023-01-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 0091-679X
    ISSN 0091-679X
    DOI 10.1016/bs.mcb.2022.12.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Targeting VCAM-1: a therapeutic opportunity for vascular damage.

    Troncoso, Mayarling F / Díaz-Vesga, Magda C / Sanhueza-Olivares, Fernanda / Riquelme, Jaime A / Müller, Marioly / Garrido, Luis / Gabrielli, Luigi / Chiong, Mario / Corbalan, Ramon / Castro, Pablo F / Lavandero, Sergio

    Expert opinion on therapeutic targets

    2023  Volume 27, Issue 3, Page(s) 207–223

    Abstract: Introduction: The vascular cell adhesion molecule (VCAM-1) is a transmembrane sialoglycoprotein detected in activated endothelial and vascular smooth muscle cells involved in the adhesion and transmigration of inflammatory cells into damaged tissue. ... ...

    Abstract Introduction: The vascular cell adhesion molecule (VCAM-1) is a transmembrane sialoglycoprotein detected in activated endothelial and vascular smooth muscle cells involved in the adhesion and transmigration of inflammatory cells into damaged tissue. Widely used as a pro-inflammatory marker, its potential role as a targeting molecule has not been thoroughly explored.
    Areas covered: We discuss the current evidence supporting the potential targeting of VCAM-1 in atherosclerosis, diabetes, hypertension and ischemia/reperfusion injury.
    Expert opinion: There is emerging evidence that VCAM-1 is more than a biomarker and may be a promising therapeutic target for vascular diseases. While there are neutralizing antibodies that allow preclinical research, the development of pharmacological tools to activate or inhibit this protein are required to thoroughly assess its therapeutic potential.
    MeSH term(s) Humans ; Vascular Cell Adhesion Molecule-1/metabolism ; Vascular Cell Adhesion Molecule-1/therapeutic use ; Atherosclerosis/drug therapy ; Endothelium, Vascular ; Reperfusion Injury
    Chemical Substances Vascular Cell Adhesion Molecule-1
    Language English
    Publishing date 2023-03-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1080/14728222.2023.2187778
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5244: Show issues Location:
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