Angiotensin-converting enzyme inhibitor treatment early after myocardial infarction attenuates acute cardiac and neuroinflammation without effect on chronic neuroinflammation

AbstractPurposeMyocardial infarction (MI) triggers a local inflammatory response which orchestrates cardiac repair and contributes to concurrent neuroinflammation. Angiotensin-converting enzyme (ACE) inhibitor therapy not only attenuates cardiac remodeling by interfering with the neurohumoral system, but also influences acute leukocyte mobilization from hematopoietic reservoirs. Here, we seek to dissect the anti-inflammatory and anti-remodeling contributions of ACE inhibitors to the benefit of heart and brain outcomes after MI.MethodsC57BL/6 mice underwent permanent coronary artery ligation (n = 41) or sham surgery (n = 9). Subgroups received ACE inhibitor enalapril (20 mg/kg, oral) either early (anti-inflammatory strategy; 10 days treatment beginning 3 days prior to surgery;n = 9) or delayed (anti-remodeling; continuous from 7 days post-MI;n = 16), or no therapy (n = 16). Cardiac and neuroinflammation were serially investigated using whole-body macrophage- and microglia-targeted translocator protein (TSPO) PET at 3 days, 7 days, and 8 weeks. In vivo PET signal was validated by autoradiography and histopathology.ResultsMyocardial infarction evoked higher TSPO signal in the infarct region at 3  days and 7 days compared with sham (p 
Source: European Journal of Nuclear Medicine and Molecular Imaging - Category: Nuclear Medicine Source Type: research

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AbstractIn the infarcted myocardium, cardiomyocyte necrosis triggers an intense inflammatory reaction that not only is critical for cardiac repair, but also contributes to adverse remodeling and to the pathogenesis of heart failure. Both CC and CXC chemokines are markedly induced in the infarcted heart, bind to endothelial glycosaminoglycans, and regulate leukocyte trafficking and function. ELR+ CXC chemokines (such as CXCL8) control neutrophil infiltration, whereas CC chemokines (such as CCL2) mediate recruitment of mononuclear cells. Moreover, some members of the chemokine family (such as CXCL10 and CXCL12) may mediate l...
Source: Journal of Cardiovascular Translational Research - Category: Cardiology Source Type: research
CONCLUSIONS: We show that resolution of cardiac inflammation after MI may be accelerated by therapeutic lymphangiogenesis based on adeno-associated viral gene delivery of VEGF-CC156S. Conversely, our work uncovers a major negative role of cardiac-recruited T cells on lymphatic remodeling. Our results give new insight into the interconnection between immune cells and lymphatics in orchestration of cardiac repair after injury. PMID: 32404007 [PubMed - as supplied by publisher]
Source: Arteriosclerosis, Thrombosis and Vascular Biology - Category: Cardiology Authors: Tags: Arterioscler Thromb Vasc Biol Source Type: research
Abstract Heart diseases remain the major cause of death worldwide. Advances in pharmacological and biomedical management have resulted in an increasing proportion of patients surviving acute heart failure (HF). However, many survivors of HF in the early stages end up increasing the disease to chronic HF (CHF). HF is an established frequent complication of myocardial infarction (MI), and numerous influences including persistent myocardial ischemia, shocked myocardium, ventricular remodeling, infarct size, and mechanical impairments, as well as hibernating myocardium trigger the development of left ventricular systo...
Source: Cardiology Research and Practice - Category: Cardiology Authors: Tags: Cardiol Res Pract Source Type: research
(University of South Florida (USF Health)) A new study by the University of South Florida Health Morsani College of Medicine and the University of Alabama at Birmingham profiled bioactive lipids in blood samples from hospitalized black and white patients soon after a heart attack. The preliminary research indicates that bioactive lipid mediators -- key to cardiac repair differences in blacks and whites after heart attack -- may offer new targets for more personalized diagnosis and treatment of heart failure.
Source: EurekAlert! - Medicine and Health - Category: International Medicine & Public Health Source Type: news
ConclusionOur comparative analyses of fatty acids and respective cyclooxygenase ‐derived and lipoxygenase‐derived SPM signatures capture the heterogeneity of disease pathology and elucidate potential mechanisms underlying sex‐based and race‐based differences following MI.
Source: ESC Heart Failure - Category: Cardiology Authors: Tags: Original Research Article Source Type: research
In conclusion, our study demonstrated that Nrf2 deficiency promoted the increasing trend of autophagy during aging in skeletal muscle. Nrf2 deficiency and increasing age may cause excessive autophagy in skeletal muscle, which can be a potential mechanism for the development of sarcopenia. To What Degree is Chondrocyte Hypertrophy in Osteoarthritis Due to Cellular Senescence? Senescent cells are large. They do not replicate, that function is disabled, but it is as if they go ...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Aging makes everything worse. Its mechanisms of damage and consequence degrade tissue function to the point of catastrophic failure, as in a heart attack. That same damage also makes the immediate consequence of a heart attack worse, and reduces regenerative capacity and the ability to respond to therapies. All in all degenerative aging is an unpleasant business, lacking an upside. The right way forward is to periodically repair the damage before it reaches a pathological level, rather than working on ways to mitigate the consequences of a sizable burden of damage. Aging elevates the susceptibility of the heart to...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs
(University of South Florida (USF Health)) A new study led by the University of South Florida Health (USF Health) Morsani College of Medicine investigated the molecular and cellular processes underlying cardiac repair in male and female mice after a severe heart attack. The researchers discovered that heart repair happened faster in the female mice than the males after heart attack, and that improved survival and delayed cardiac failure.
Source: EurekAlert! - Medicine and Health - Category: International Medicine & Public Health Source Type: news
In conclusion, elevated brain amyloid was associated with family history and APOE ε4 allele but not with multiple other previously reported risk factors for AD. Elevated amyloid was associated with lower test performance results and increased reports of subtle recent declines in daily cognitive function. These results support the hypothesis that elevated amyloid represents an early stage in the Alzheimer's continuum. Blood Metabolites as a Marker of Frailty Frailty in older people is usually diagnosed in a sympt...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
AbstractThe spectrum of ischemic heart diseases, encompassing acute myocardial infarction to heart failure, represents the leading cause of death worldwide. Although extensive progress in cardiovascular diagnoses and therapy has been made, the prevalence of the disease continues to increase. Cardiac regeneration has a promising perspective for the therapy of heart failure. Recently, extracellular matrix (ECM) has been shown to play an important role in cardiac regeneration and repair after cardiac injury. There is also evidence that the ECM could be directly used as a drug to promote cardiomyocyte proliferation and cardiac...
Source: Heart Failure Reviews - Category: Cardiology Source Type: research
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