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  1. AU="Khlestkina, Maria S"
  2. AU="Ebina-Shibuya, Risa"
  3. AU="Vogel, Ida"
  4. AU="Facchiano, Angelo"
  5. AU="Tara Rava Zolnikov"
  6. AU="Akther, Tahmina"
  7. AU=Chung Eugene S
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  1. Artikel: Apelin Is a Prototype of Novel Drugs for the Treatment of Acute Myocardial Infarction and Adverse Myocardial Remodeling.

    Popov, Sergey V / Maslov, Leonid N / Mukhomedzyanov, Alexandr V / Kurbatov, Boris K / Gorbunov, Alexandr S / Kilin, Michail / Azev, Viacheslav N / Khlestkina, Maria S / Sufianova, Galina Z

    Pharmaceutics

    2023  Band 15, Heft 3

    Abstract: In-hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is 5-6%. Consequently, it is necessary to develop fundamentally novel drugs capable of reducing mortality in patients with acute myocardial infarction. Apelins ... ...

    Abstract In-hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is 5-6%. Consequently, it is necessary to develop fundamentally novel drugs capable of reducing mortality in patients with acute myocardial infarction. Apelins could be the prototype for such drugs. Chronic administration of apelins mitigates adverse myocardial remodeling in animals with myocardial infarction or pressure overload. The cardioprotective effect of apelins is accompanied by blockage of the MPT pore, GSK-3β, and the activation of PI3-kinase, Akt, ERK1/2, NO-synthase, superoxide dismutase, glutathione peroxidase, matrix metalloproteinase, the epidermal growth factor receptor, Src kinase, the mitoK
    Sprache Englisch
    Erscheinungsdatum 2023-03-22
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2527217-2
    ISSN 1999-4923
    ISSN 1999-4923
    DOI 10.3390/pharmaceutics15031029
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Pharmacological Approaches to Limit Ischemic and Reperfusion Injuries of the Heart: Analysis of Experimental and Clinical Data on P2Y

    Maslov, Leonid N / Popov, Sergey V / Mukhomedzyanov, Alexandr V / Derkachev, Ivan A / Ryabov, Vyacheslav V / Boshchenko, Alla A / Prasad, N Rajendra / Sufianova, Galina Z / Khlestkina, Maria S / Gareev, Ilgiz

    Korean circulation journal

    2022  Band 52, Heft 10, Seite(n) 737–754

    Abstract: Ischemic and reperfusion injuries of the heart underlie the pathogenesis of acute myocardial infarction (AMI) and sudden cardiac death. The mortality rate is still high and is 5-7% in patients with ST-segment elevation myocardial infarction. The review ... ...

    Abstract Ischemic and reperfusion injuries of the heart underlie the pathogenesis of acute myocardial infarction (AMI) and sudden cardiac death. The mortality rate is still high and is 5-7% in patients with ST-segment elevation myocardial infarction. The review is devoted to pharmacological approaches to limitation of ischemic and reperfusion injuries of the heart. The article analyzes experimental evidence and the clinical data on the effects of P2Y
    Sprache Englisch
    Erscheinungsdatum 2022-10-10
    Erscheinungsland Korea (South)
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2557464-4
    ISSN 1738-5520
    ISSN 1738-5520
    DOI 10.4070/kcj.2022.0162
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Regulation of autophagy of the heart in ischemia and reperfusion.

    Popov, Sergey V / Mukhomedzyanov, Alexander V / Voronkov, Nikita S / Derkachev, Ivan A / Boshchenko, Alla A / Fu, Feng / Sufianova, Galina Z / Khlestkina, Maria S / Maslov, Leonid N

    Apoptosis : an international journal on programmed cell death

    2022  Band 28, Heft 1-2, Seite(n) 55–80

    Abstract: Ischemia/reperfusion (I/R) of the heart leads to increased autophagic flux. Preconditioning stimulates autophagic flux by AMPK and PI3-kinase activation and mTOR inhibition. The cardioprotective effect of postconditioning is associated with activation of ...

    Abstract Ischemia/reperfusion (I/R) of the heart leads to increased autophagic flux. Preconditioning stimulates autophagic flux by AMPK and PI3-kinase activation and mTOR inhibition. The cardioprotective effect of postconditioning is associated with activation of autophagy and increased activity of NO-synthase and AMPK. Oxidative stress stimulates autophagy in the heart during I/R. Superoxide radicals generated by NADPH-oxidase acts as a trigger for autophagy, possibly due to AMPK activation. There is reason to believe that AMPK, GSK-3β, PINK1, JNK, hexokinase II, MEK, PKCα, and ERK kinases stimulate autophagy, while mTOR, PKCδ, Akt, and PI3-kinase can inhibit autophagy in the heart during I/R. However, there is evidence that PI3-kinase could stimulate autophagy in ischemic preconditioning of the heart. It was found that transcription factors FoxO1, FoxO3, NF-κB, HIF-1α, TFEB, and Nrf-2 enhance autophagy in the heart in I/R. Transcriptional factors STAT1, STAT3, and p53 inhibit autophagy in I/R. MicroRNAs could stimulate and inhibit autophagy in the heart in I/R. Long noncoding RNAs regulate the viability and autophagy of cardiomyocytes in hypoxia/reoxygenation (H/R). Nitric oxide (NO) donors and endogenous NO could activate autophagy of cardiomyocytes. Activation of heme oxygenase-1 promotes cardiomyocyte tolerance to H/R and enhances autophagy. Hydrogen sulfide increases cardiac tolerance to I/R and inhibits apoptosis and autophagy via mTOR and PI3-kinase activation.
    Mesh-Begriff(e) Humans ; Signal Transduction ; AMP-Activated Protein Kinases/metabolism ; Glycogen Synthase Kinase 3 beta ; Apoptosis ; TOR Serine-Threonine Kinases/metabolism ; Myocytes, Cardiac/metabolism ; Myocardial Reperfusion Injury ; Ischemia ; Reperfusion ; Autophagy ; Phosphatidylinositol 3-Kinases
    Chemische Substanzen AMP-Activated Protein Kinases (EC 2.7.11.31) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
    Sprache Englisch
    Erscheinungsdatum 2022-11-11
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1452360-7
    ISSN 1573-675X ; 1360-8185
    ISSN (online) 1573-675X
    ISSN 1360-8185
    DOI 10.1007/s10495-022-01786-1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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