We are analyzing https://link.springer.com/article/10.1007/s11897-022-00539-0.

Title:
Mitochondria as Therapeutic Targets in Heart Failure | Current Heart Failure Reports
Description:
Purpose of Review We review therapeutic approaches aimed at restoring function of the failing heart by targeting mitochondrial reactive oxygen species (ROS), ion handling, and substrate utilization for adenosine triphosphate (ATP) production. Recent Findings Mitochondria-targeted therapies have been tested in animal models of and humans with heart failure (HF). Cardiac benefits of sodium/glucose cotransporter 2 inhibitors might be partly explained by their effects on ion handling and metabolism of cardiac myocytes. Summary The large energy requirements of the heart are met by oxidative phosphorylation in mitochondria, which is tightly regulated by the turnover of ATP that fuels cardiac contraction and relaxation. In heart failure (HF), this mechano-energetic coupling is disrupted, leading to bioenergetic mismatch and production of ROS that drive the progression of cardiac dysfunction. Furthermore, HF is accompanied by changes in substrate uptake and oxidation that are considered detrimental for mitochondrial oxidative metabolism and negatively affect cardiac efficiency. Mitochondria lie at the crossroads of metabolic and energetic dysfunction in HF and represent ideal therapeutic targets.
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Keywords {🔍}

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Topics {✒️}

pressure-overload-induced heart failure article download pdf mitochondria-targeted cytoprotective peptides long-chain 3-ketoacyl coenzyme mitochondria-targeting cytoprotective peptide malonyl-coa decarboxylase inhibitors 36-week open-label extension reactive oxygen species mitochondria-targeting peptide bendavia digoxin accelerate ca2+ efflux malonyl-coa levels dictate targeting mitochondria-inflammation circuit sarcolemmal sodium-hydrogen exchanger mitochondria-targeted antioxidant mitoq empa-reg outcome trial microembolization-induced heart failure angiotensin ii-induced cardiomyopathy malonyl-coa decarboxylase provide manganese-dependent superoxide dismutase randomized dose-escalation trial pressure overload–induced hf sodium-hydrogen exchange inhibition fatty acid β-oxidation x-linked gene open access published increasing malonyl-coa levels extracellular na+-binding site myocardial ischemia/reperfusion injury mitochondrial na+/ca2+ exchanger sarcolemmal na+/ca2+ exchanger sarcolemmal na+/ca2+ exchanger late sodium current optimal medical therapy energy-starved failing heart high-risk ischemic situations mitochondrial-targeted peptides β-ohb oxidation requires l-type ca2+ channels directly inhibiting β-oxidation β-hydroxybutyrate mitigates hfpef late na+ current altered mechano-energetic coupling percutaneous coronary intervention lv end-systolic volume significant dose-dependent improvement krebs cycle-mediated regeneration mitochondria-targeting peptide elevated cytosolic sodium restoring mechano-energetic coupling general cellular—ros formation

Schema {🗺️}

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         headline:Mitochondria as Therapeutic Targets in Heart Failure
         description:We review therapeutic approaches aimed at restoring function of the failing heart by targeting mitochondrial reactive oxygen species (ROS), ion handling, and substrate utilization for adenosine triphosphate (ATP) production. Mitochondria-targeted therapies have been tested in animal models of and humans with heart failure (HF). Cardiac benefits of sodium/glucose cotransporter 2 inhibitors might be partly explained by their effects on ion handling and metabolism of cardiac myocytes. The large energy requirements of the heart are met by oxidative phosphorylation in mitochondria, which is tightly regulated by the turnover of ATP that fuels cardiac contraction and relaxation. In heart failure (HF), this mechano-energetic coupling is disrupted, leading to bioenergetic mismatch and production of ROS that drive the progression of cardiac dysfunction. Furthermore, HF is accompanied by changes in substrate uptake and oxidation that are considered detrimental for mitochondrial oxidative metabolism and negatively affect cardiac efficiency. Mitochondria lie at the crossroads of metabolic and energetic dysfunction in HF and represent ideal therapeutic targets.
         datePublished:2022-02-11T00:00:00Z
         dateModified:2022-02-11T00:00:00Z
         pageStart:27
         pageEnd:37
         license:http://creativecommons.org/licenses/by/4.0/
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            Heart failure
            Reactive oxygen species
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            SGLT2 inhibitors
            Cardiac metabolism
            Cardiology
            Cardiac Surgery
            Vascular Surgery
            Internal Medicine
            Imaging / Radiology
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ScholarlyArticle:
      headline:Mitochondria as Therapeutic Targets in Heart Failure
      description:We review therapeutic approaches aimed at restoring function of the failing heart by targeting mitochondrial reactive oxygen species (ROS), ion handling, and substrate utilization for adenosine triphosphate (ATP) production. Mitochondria-targeted therapies have been tested in animal models of and humans with heart failure (HF). Cardiac benefits of sodium/glucose cotransporter 2 inhibitors might be partly explained by their effects on ion handling and metabolism of cardiac myocytes. The large energy requirements of the heart are met by oxidative phosphorylation in mitochondria, which is tightly regulated by the turnover of ATP that fuels cardiac contraction and relaxation. In heart failure (HF), this mechano-energetic coupling is disrupted, leading to bioenergetic mismatch and production of ROS that drive the progression of cardiac dysfunction. Furthermore, HF is accompanied by changes in substrate uptake and oxidation that are considered detrimental for mitochondrial oxidative metabolism and negatively affect cardiac efficiency. Mitochondria lie at the crossroads of metabolic and energetic dysfunction in HF and represent ideal therapeutic targets.
      datePublished:2022-02-11T00:00:00Z
      dateModified:2022-02-11T00:00:00Z
      pageStart:27
      pageEnd:37
      license:http://creativecommons.org/licenses/by/4.0/
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      keywords:
         Mitochondria
         Heart failure
         Reactive oxygen species
         MitoQ
         Elamipretide
         SGLT2 inhibitors
         Cardiac metabolism
         Cardiology
         Cardiac Surgery
         Vascular Surgery
         Internal Medicine
         Imaging / Radiology
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         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11897-022-00539-0/MediaObjects/11897_2022_539_Fig1_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11897-022-00539-0/MediaObjects/11897_2022_539_Fig2_HTML.png
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               type:PostalAddress
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               name:Department of Internal Medicine and Specialties (Di.M.I.), University of Genoa, Genoa, Italy
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      name:Department of Translational Research, Comprehensive Heart Failure Center, University Clinic Würzburg, Würzburg, Germany
      name:Department of Translational Research, Comprehensive Heart Failure Center, University Clinic Würzburg, Würzburg, Germany
      name:Department of Translational Research, Comprehensive Heart Failure Center, University Clinic Würzburg, Würzburg, Germany
      name:Department of Internal Medicine and Specialties (Di.M.I.), University of Genoa, Genoa, Italy

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