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Impact of impaired renal function on kinetics of high-sensitive cardiac troponin following cardiac surgery.
Clin Res Cardiol
January 2025
Clinic for General and Interventional Cardiology/Angiology, Herz- und Diabeteszentrum NRW, Ruhr-Universität Bochum, Georgstraße 11, 32545, Bad Oeynhausen, Germany.
Background: Impaired renal function can increase cardiac troponin levels due to reduced elimination, potentially affecting its diagnostic utility. Limited data exist on high-sensitivity cardiac troponin I (hs-cTnI) kinetics after cardiac surgery relative to renal function. This study evaluates how impaired renal function influences hs-cTnI kinetics following cardiac surgery, distinguishing between patients with and without postoperative myocardial infarction (PMI).
View Article and Find Full Text PDFThermosensitive Porcine Myocardial Extracellular Matrix Hydrogel Coupled with Proanthocyanidins for Cardiac Tissue Engineering.
Gels
January 2025
Laboratory of Immunotherapy and Tissue Engineering, Department of Cellular and Tissue Biology, Faculty of Medicine, National Autonomous University of Mexico, Av. Universidad 3000, Copilco Universidad, Coyoacán, Ciudad de México 04510, Mexico.
Currently, there are no therapies that prevent the negative myocardial remodeling process that occurs after a heart attack. Injectable hydrogels are a treatment option because they may replace the damaged extracellular matrix and, in addition, can be administered minimally invasively. Reactive oxygen species generated by ischemia-reperfusion damage can limit the therapeutic efficacy of injectable hydrogels.
View Article and Find Full Text PDFSulfated and Phosphorylated Agarose as Biomaterials for a Biomimetic Paradigm for FGF-2 Release.
Biomimetics (Basel)
December 2024
Institute for Macromolecular Chemistry, Stefan-Meier-Strasse 31, 79104 Freiburg, Germany.
Cardiovascular diseases such as myocardial infarction or limb ischemia are characterized by regression of blood vessels. Local delivery of growth factors (GFs) involved in angiogenesis such as fibroblast blast growth factor-2 (FGF-2) has been shown to trigger collateral neovasculature and might lead to a therapeutic strategy. In vivo, heparin, a sulfated polysaccharide present in abundance in the extracellular matrix (ECM), has been shown to function as a local reservoir for FGF-2 by binding FGF-2 and other morphogens and it plays a role in the evolution of GF gradients.
View Article and Find Full Text PDFProlonged Hypoxia in Rat Living Myocardial Slices Affects Function, Expression, and Structure.
Int J Mol Sci
December 2024
Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, 30625 Hannover, Germany.
Ischemic heart disease is the leading cause of death worldwide. Reduced oxygen supply and myocardial hypoxia lead to tissue damage and impairment of the heart function. To the best of our knowledge, the primary functional effects of hypoxia in the multicellular model of living myocardial slices (LMSs) have not been investigated so far.
View Article and Find Full Text PDFThe N-Terminal Mutations of cMyBP-C Affect Calcium Regulation, Kinetics, and Force of Muscle Contraction.
Int J Mol Sci
December 2024
Institute of Immunology and Physiology, Russian Academy of Sciences, 620049 Yekaterinburg, Russia.
The cardiac myosin binding protein-C (cMyBP-C) regulates cross-bridge formation and controls the duration of systole and diastole at the whole heart level. As known, mutations in cMyBP-C increase the cross-bridge number and rate of their cycling, hypercontractility, and myocardial hypertrophy. We investigated the effects of the mutations D75N and P161S of cMyBP-C related to hypertrophic cardiomyopathy on the mechanism of force generation in isolated slow skeletal muscle fibers.
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