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Assessment of myocardialInfarctionCardiacProtects the heartInfarct sizeInflammationViabilityVascularIschemicProtectiveSalvageTissueAcuteMechanismsChronicProtectionStressInfarction and strokeOxidative stressProgressionHypertensionStrokeDilated cardiomyopathyMiceCardiovascularDiabeticOccurImmuneInflammatory responsesTissue injuryRestorationHeart failureLung injuryModelAdditionalEventsActivation

Assessment of myocardial1

• Its applications include assessment of myocardial ischemia and viability, cardiomyopathies, myocarditis , iron overload , vascular diseases and congenital heart disease . (alchetron.com)

Infarction1

• Stroke and myocardial infarction are among the most common causes of mortality and disability in the world. (cdc.gov)

Cardiac3

• In addition to its function in skeletal muscle, MG53 has been shown to have protective effects on various forms of cardiac muscle injury. (biomedcentral.com)
• Cardiac ischemia is modelled in vitro through the application of hypoxic and oxidative stress. (biomedcentral.com)
• Nakamura K, Sano S, Fuster JJ, Kikuchi R, Shimizu I, Ohshima K, Katanasaka Y, Ouchi N, Walsh K. Secreted Frizzled-related Protein 5 Diminishes Cardiac Inflammation and Protects the Heart from Ischemia/Reperfusion Injury. (bu.edu)

Protects the heart1

• Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)

Infarct size1

• MG53 KO mice lack IPC-mediated cardioprotection as evidenced by a failure of IPC to reduce IR-induced myocardial infarct size. (biomedcentral.com)

Inflammation2

• Oxidative stress is a strong contributing factor to cardiovascular disease, and often occurs because of inflammation caused by ischemia reperfusion injury. (wikipedia.org)
• The ischemic injury underlying these illnesses is complex, involving intricate interplays among many biological functions including energy metabolism, vascular regulation, hemodynamics, oxidative stress, inflammation, platelet activation, and tissue repair that take place in a context- and time-dependent manner. (cdc.gov)

Viability1

• Since cardiomyocytes are terminally differentiated cells with limited self-renewal capacity, and membrane rupture is a major cause of cardiomyocyte cell death following injury, membrane repair is a necessary process for preserving cardiomyocyte viability [ 6 ]. (biomedcentral.com)

Vascular1

• Based on our work to date, we are also interested in understanding myocardial mitochondrial and vascular dysfunction as these have the potential to serve as novel therapeutic targets. (stanford.edu)

Ischemic1

• and is an intrinsic process through which repeated short episodes of ischemia are instituted to protect the myocardium against subsequent ischemic insults [ 7 ]. (biomedcentral.com)

Protective1

• However, accumulating evidence suggests that MG53 has a potentially protective role in heart tissue, including in ischemia/reperfusion injury of the heart, cardiomyocyte membrane injury repair, and atrial fibrosis. (biomedcentral.com)

Salvage1

• IPC activates the reperfusion injury salvage kinase (RISK) and survivor activating factor enhancement (SAFE) pathways to protect the heart against IR injury. (biomedcentral.com)

Tissue1

• but reperfusion may introduce additional harm to the tissue through a process known as ischemia/reperfusion injury. (cdc.gov)

Acute1

• Adiponectin attenuates lipopolysaccharide-induced acute lung injury through suppression of endothelial cell activation. (bu.edu)

Mechanisms1

• My laboratory's overall goal is to (i) understand the mechanisms of right heart failure in children and adults with congenital heart disease and (ii) to develop biomarkers as a plasma signature of myocardial events to better understand the mechanisms of heart failure, improve monitoring of disease progression, early detection of heart failure and risk-stratification. (stanford.edu)

Chronic1

• Here we review the current literature on scutellarin to provide a comprehensive understanding of the pharmacological activity, mechanism of action, toxicity, and therapeutic potential of scutellarin for the treatment of ischemia, diabetic complications, and other chronic diseases. (cdc.gov)

Protection2

• Above all, PGRN also provides protection in the initial phase following myocardial ischemia-reperfusion injury. (biomedcentral.com)
• As such, new drugs that would complement reperfusion by providing neural and cardiovascular protection and by targeting multiple abnormalities in ischemia are receiving increased attention. (cdc.gov)

Stress1

• Ischemia/reperfusion (I/R) in mouse hearts and hypoxia/oxidative stress in neonatal rat cardiomyocytes have been associated with a downregulation of MG53. (biomedcentral.com)

Infarction and stroke1

• A meta-analysis of 11 small, low-quality studies concludes that coenzyme Q10 probably reduces risk of all-cause and cardiovascular mortality, and of hospital admission for CHF, but data on improvement in LVEF or exercise capacity and the risk for myocardial infarction and stroke are inconclusive. (therapeuticresearch.com)

Oxidative stress2

• Oxidative stress is a strong contributing factor to cardiovascular disease, and often occurs because of inflammation caused by ischemia reperfusion injury. (wikipedia.org)
• The ischemic injury underlying these illnesses is complex, involving intricate interplays among many biological functions including energy metabolism, vascular regulation, hemodynamics, oxidative stress, inflammation, platelet activation, and tissue repair that take place in a context- and time-dependent manner. (cdc.gov)

Progression2

• Myofilament Ca 2+ sensitivity correlates with left ventricular contractility during the progression of pressure overload-induced left ventricular myocardial hypertrophy in rats. (uni-heidelberg.de)
• Interleukin-17A is dispensable for myocarditis but essential for the progression to dilated cardiomyopathy. (zju.edu.cn)

Hypertension1

• Here, in this review, we will discuss recent updates on the regulatory role of microglia in hypertension, myocardial infarction and ischemia/reperfusion injury. (nih.gov)

Stroke1

• Stroke and myocardial infarction are among the most common causes of mortality and disability in the world. (cdc.gov)

Dilated cardiomyopathy2

• These immune cells can cause myocarditis which can progress to dilated cardiomyopathy and heart failure. (wikipedia.org)
• Case summary: A 66-year-old patient with known dilated cardiomyopathy was admitted with non-ST-elevation myocardial infarction and underwent urgent coronary bypass grafting. (bvsalud.org)

Mice3

• Ventilator-induced lung injury is aggravated by antibiotic mediated microbiota depletion in mice. (medscape.com)
• A Minimal-Invasive Approach for Standardized Induction of Myocardial Infarction in Mice. (uni-heidelberg.de)
• C57BL/6) and ACE2 KO mice (ACE2 -/- ) were utilized to study CS-induced lung injury. (ijbs.com)

Cardiovascular1

• As such, new drugs that would complement reperfusion by providing neural and cardiovascular protection and by targeting multiple abnormalities in ischemia are receiving increased attention. (cdc.gov)

Diabetic1

• The extent of injury was extensive in diabetic groups if compared to non-diabetic groups. (eurjanat.com)

Occur1

• Expression of TSPO is also linked to inflammatory responses that occur after ischemia-reperfusion injury, following hemorrhagic brain injury, and in some neurodegenerative diseases. (wikipedia.org)

Immune2

• Heart-Specific Immune Responses in an Animal Model of Autoimmune-Related Myocarditis Mitigated by an Immunoproteasome Inhibitor and Genetic Ablation. (uni-heidelberg.de)
• Many etiological processes have been suggested: viral myocarditis, abnormal immune response to pregnancy, excessive prolactin excretion, prolonged tocolysis and a familiar predisposition to PPCM. (lakotalakes.com)

Inflammatory responses1

• citation needed] Increased expression of TSPO is linked to the inflammatory responses in the heart that may cause myocarditis, which can lead to myocardial necrosis. (wikipedia.org)

Tissue injury2

• CASP-3 gene plays an important role in trace-metal-associated tissue injury. (eurjanat.com)
• Iatrogenic revascularization and restoration of perfusion results paradoxically in aggravated tissue injury. (bvsalud.org)

Restoration1

• Although restoration of blood flow to the jeopardized myocardium is a perquisite for myocardial salvage, reperfusion itself may lead to accelerated and additional myocardial injury, termed reperfusion injury, beyond that generated by ischemia alone. (nih.gov)

Heart failure1

• Pharmacological therapies other than angiotensin-converting enzyme inhibitors and beta-blockers, aimed at attenuating left ventricular remodeling and preventing the development of heart failure, are critical to progress. (nih.gov)

Lung injury3

• However, the relationship between ACE2 and MMPs activation in lung injury is still largely unclear. (ijbs.com)
• The purpose of this study is to investigate whether MMPs activity could be affected by ACE2 and which ACE2 derived signaling pathways could be also involved via using a mouse model with lung injury induced by cigarette smoke (CS) exposure for 1 to 3 weeks. (ijbs.com)
• In addition, matrix metalloproteinases (MMPs) have also been demonstrated to be strongly associated with the lung injury [ 9 ], and could be regulated by MAKP signaling as well as signal transducer and activator of transcription 3 (STAT3) pathways [ 10 , 11 ]. (ijbs.com)

Model2

• This chapter will provide a detailed experimental setup and a step-by-step protocol for the dynamic imaging of leukocyte-endothelial-interaction in an ischemia/reperfusion injury model. (bvsalud.org)
• IL-17A levels increase in the infarcted region of the left ventricle in a rat model of myocardial infarction. (zju.edu.cn)

Additional1

• but reperfusion may introduce additional harm to the tissue through a process known as ischemia/reperfusion injury. (cdc.gov)

Events1

• As the heart responds to such an injury, various critical events are initiated. (nih.gov)

Activation1

• CaMKII activation participates in doxorubicin cardiotoxicity and is attenuated by moderate GRP78 overexpression. (uni-heidelberg.de)