Imaging, Biomarker, and Clinical Predictors of Cardiac Remodeling in Heart Failure With Reduced Ejection Fraction

JACC Heart Failure, Journal Year: 2019, Volume and Issue: 7(9), P. 782 - 794

Published: Aug. 7, 2019

Language: Английский

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Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets

Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)

Published: Jan. 8, 2024

Abstract Ischemia-reperfusion (I/R) injury paradoxically occurs during reperfusion following ischemia, exacerbating the initial tissue damage. The limited understanding of intricate mechanisms underlying I/R hinders development effective therapeutic interventions. Wnt signaling pathway exhibits extensive crosstalk with various other pathways, forming a network system pathways involved in injury. This review article elucidates signaling, as well complex interplay between and including Notch, phosphatidylinositol 3-kinase/protein kinase B, transforming growth factor-β, nuclear factor kappa, bone morphogenetic protein, N-methyl-D-aspartic acid receptor-Ca 2+ -Activin A, Hippo-Yes-associated toll-like receptor 4/toll-interleukine-1 domain-containing adapter-inducing interferon-β, hepatocyte factor/mesenchymal-epithelial transition factor. In particular, we delve into their respective contributions to key pathological processes, apoptosis, inflammatory response, oxidative stress, extracellular matrix remodeling, angiogenesis, cell hypertrophy, fibrosis, ferroptosis, neurogenesis, blood-brain barrier damage Our comprehensive analysis reveals that activation canonical promotes organ recovery, while non-canonical exacerbates Moreover, explore novel approaches based on these mechanistic findings, incorporating evidence from animal experiments, current standards, clinical trials. objective this is provide deeper insights roles its I/R-mediated processes dysfunction, facilitate innovative agents for

Language: Английский

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The role of mitochondrial fission in cardiovascular health and disease

Nature Reviews Cardiology, Journal Year: 2022, Volume and Issue: 19(11), P. 723 - 736

Published: May 6, 2022

Language: Английский

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Phosphoenolpyruvate carboxykinase in cell metabolism: Roles and mechanisms beyond gluconeogenesis

Molecular Metabolism, Journal Year: 2021, Volume and Issue: 53, P. 101257 - 101257

Published: May 18, 2021

Phosphoenolpyruvate carboxykinase (PCK) has been almost exclusively recognized as a critical enzyme in gluconeogenesis, especially the liver and kidney. Accumulating evidence shown that enhanced activity of PCK leads to increased glucose output exacerbation diabetes, whereas defects result lethal hypoglycemia. Genetic mutations or polymorphisms are reported be related onset progression diabetes humans.

Language: Английский

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Resident cardiac macrophages mediate adaptive myocardial remodeling

Immunity, Journal Year: 2021, Volume and Issue: 54(9), P. 2072 - 2088.e7

Published: July 27, 2021

Language: Английский

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Lycopene in the Prevention of Cardiovascular Diseases

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(4), P. 1957 - 1957

Published: Feb. 10, 2022

Cardiovascular diseases (CVDs) are the leading cause of human mortality worldwide. Oxidative stress and inflammation pathophysiological processes involved in development CVD. That is why bioactive food ingredients, including lycopene, so important their prevention, which seems to be a compound increasingly promoted diet people with cardiovascular problems. Lycopene present tomatoes tomato products responsible not only for red color but also health-promoting properties. It characterized by high antioxidant potential, highest among carotenoid pigments. Mainly this reason, epidemiological studies show number favorable properties between consumption lycopene reduced risk disease. While there some controversy research into its protective effects on system, growing evidence supports beneficial role heart, endothelium, blood vessels, health. The mechanisms action now being discovered may explain contradictions observed literature. This review aims current knowledge recent years preventive disorders.

Language: Английский

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Oxidative Stress as A Mechanism for Functional Alterations in Cardiac Hypertrophy and Heart Failure

Antioxidants, Journal Year: 2021, Volume and Issue: 10(6), P. 931 - 931

Published: June 8, 2021

Although heart failure due to a wide variety of pathological stimuli including myocardial infarction, pressure overload and volume is associated with cardiac hypertrophy, the exact reasons for transition hypertrophy are not well defined. Since circulating levels several vasoactive hormones catecholamines, angiotensin II, endothelins elevated under conditions, it has been suggested that these may be involved in development both failure. At initial stages stimuli, induce an increase ventricular wall tension by acting through their respective receptor-mediated signal transduction systems result hypertrophy. Some oxyradicals formed at also redox-dependent activation hypertrophic process but rapidly removed increased content antioxidants hypertrophied heart. In fact, considered adaptive as exhibits either normal or augmented function maintaining cardiovascular homeostasis. However, exposure over prolonged period results dysfunction involving complex set mechanisms. It demonstrated different abnormalities such functional hypoxia, metabolic derangements, uncoupling mitochondrial electron transport, inflammation produce oxidative stress failing hearts. addition, oxidation catecholamines monoamine oxidase NADPH II endothelin promote generation during stimuli. noteworthy known activate metallomatrix proteases degrade extracellular matrix proteins induction remodeling dysfunction. Furthermore, shown subcellular Ca2+-handling loss cardiomyocytes apoptosis, necrosis, fibrosis. These observations support view low amount oxyradical formation brief redox-sensitive mechanisms, which On other hand, high cause defects protease thus play critical role adverse progression

Language: Английский

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Exercise sustains the hallmarks of health

Journal of sport and health science/Journal of Sport and Health Science, Journal Year: 2022, Volume and Issue: 12(1), P. 8 - 35

Published: Oct. 29, 2022

Exercise has long been known for its active role in improving physical fitness and sustaining health. Regular moderate-intensity exercise improves all aspects of human health is widely accepted as a preventative therapeutic strategy various diseases. It well-documented that maintains restores homeostasis at the organismal, tissue, cellular, molecular levels to stimulate positive physiological adaptations consequently protect against pathological conditions. Here we mainly summarize how affects major hallmarks health, including integrity barriers, containment local perturbations, recycling turnover, integration circuitries, rhythmic oscillations, homeostatic resilience, hormetic regulation, well repair regeneration. Furthermore, current understanding mechanisms responsible beneficial response exercise. This review aimed providing comprehensive summary vital biological through which opens window application other interventions. We hope continuing investigation this field will further increase our processes involved thus get us closer identification new therapeutics improve quality life.

Language: Английский

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Extracellular vesicles in cardiovascular disease: Biological functions and therapeutic implications

Pharmacology & Therapeutics, Journal Year: 2021, Volume and Issue: 233, P. 108025 - 108025

Published: Oct. 21, 2021

Language: Английский

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YAP mediates compensatory cardiac hypertrophy through aerobic glycolysis in response to pressure overload

Journal of Clinical Investigation, Journal Year: 2022, Volume and Issue: 132(6)

Published: Feb. 8, 2022

The heart utilizes multiple adaptive mechanisms to maintain pump function. Compensatory cardiac hypertrophy reduces wall stress and oxygen consumption, thereby protecting the against acute blood pressure elevation. nuclear effector of Hippo pathway, Yes-associated protein 1 (YAP), is activated mediates compensatory in response overload (PO). In this study, YAP promoted glycolysis by upregulating glucose transporter (GLUT1), which turn caused accumulation intermediates metabolites glycolytic, auxiliary, anaplerotic pathways during PO. Cardiac was inhibited failure exacerbated mice with haploinsufficiency presence However, normalization GLUT1 rescued detrimental phenotype. PO induced glycolytic metabolites, including l-serine, l-aspartate, malate, a YAP-dependent manner, promoting hypertrophy. upregulated gene through interaction TEA domain family member (TEAD1) HIF-1α cardiomyocytes. Thus, induces activation Warburg effect.

Language: Английский

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