The speed of healing of myocardial infarction

Mallory, G. Kenneth; White, Paul D.; Salcedo-Salgar, Jorge

doi:10.1016/s0002-8703(39)90845-8

Cited by 683 publications

(14 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…38 Further, ISGs under the control of cGAS (Figure 1) are among the most highly down-regulated genes during macrophage polarization from M1 to M2. 39 This, coupled with the established phagocytic nature of macrophages targeting damaged myocardium, 10, 40 suggested to us that cGAS-STING pathway activation may play a role in the transition of macrophage pools from an activated/inflammatory (M1-like) subtype to the activated/reparative (M2-like) subtype. To test this hypothesis, we harvested bone marrow-derived macrophages (BMDM) and evaluated their M1 versus M2 phenotype after they were challenged with DNA.…”

Section: Resultsmentioning

confidence: 97%

Cytosolic DNA Sensing Promotes Macrophage Transformation and Governs Myocardial Ischemic Injury

Cao

Schiattarella²,

Villalobos³

et al. 2018

Circulation

174

137

View full text Add to dashboard Cite

Background Myocardium irreversibly injured by ischemic stress must be efficiently repaired to maintain tissue integrity and contractile performance. Macrophages play critical roles in this process. These cells transform across a spectrum of phenotypes to accomplish diverse functions ranging from mediating the initial inflammatory responses that clear damaged tissue to subsequent reparative functions that help rebuild replacement tissue. Although macrophage transformation is crucial to myocardial repair, events governing this transformation are poorly understood. Methods Here, we set out to determine whether innate immune responses triggered by cytoplasmic DNA play a role. Results We report that ischemic myocardial injury, and the resulting release of nucleic acids, activates the recently described cGAS (GMP-AMP synthase)-STING (stimulator of interferon genes) pathway. Animals lacking cGAS display significantly improved early survival post-MI, diminished pathological remodeling including ventricular rupture, enhanced angiogenesis, and preserved ventricular contractile function. Furthermore, cGAS loss-of-function abolishes the induction of key inflammatory programs such as iNOS and promotes the transformation of macrophages to a reparative phenotype, which results in enhanced repair and improved hemodynamic performance. Conclusions These results reveal, for the first time, that the cytosolic DNA receptor cGAS functions during cardiac ischemia as a pattern recognition receptor in the sterile immune response. Further, we report that this pathway governs macrophage transformation, thereby regulating post-injury cardiac repair. As modulators of this pathway are currently in clinical use, our findings raise the prospect of new treatment options to combat ischemic heart disease and its progression to heart failure.

show abstract

Section: Resultsmentioning

confidence: 97%

Cytosolic DNA Sensing Promotes Macrophage Transformation and Governs Myocardial Ischemic Injury

Cao

Schiattarella²,

Villalobos³

et al. 2018

Circulation

174

137

View full text Add to dashboard Cite

show abstract

“…The relationship between inflammation and myocardial infarction (MI) was suggested more than 50 years ago. 1 Since then, overwhelming evidences supporting this relationship have been obtained from various basic sciences, epidemiological and clinical studies. 2 - 4 …”

Section: Introductionmentioning

confidence: 97%

The Predictive Value of Total Neutrophil Count and Neutrophil/ Lymphocyte Ratio in Predicting In-hospital Mortality and Complications after STEMI

Ghaffari

Nadiri²,

Pourafkari

et al. 2014

Journal of Cardiovascular and Thoracic Research; ISSN 2008-6830

View full text Add to dashboard Cite

“… 3 The relationship between inflammation and MI was suggested more than 50 years ago. 4 Since then overwhelming evidences supporting that inflammation plays a key role in coronary artery disease (CAD) and other manifestations of atherosclerosis have emerged. 4 , 5 , 6 , 7 Immune cells dominate early atherosclerotic lesions, their effector molecules accelerate progression of the lesions, and activation of inflammation may lead to ACS.…”

Section: Introductionmentioning

confidence: 99%

“… 4 Since then overwhelming evidences supporting that inflammation plays a key role in coronary artery disease (CAD) and other manifestations of atherosclerosis have emerged. 4 , 5 , 6 , 7 Immune cells dominate early atherosclerotic lesions, their effector molecules accelerate progression of the lesions, and activation of inflammation may lead to ACS. 8 Neutrophils are speculated to mediate plaque rupture and thrombosis by secreting proteolytic enzymes causing vascular damage, activation of coagulation pathways, micro vascular plugging and myocyte necrosis, mediated by secretion of pro-inflammatory cytokines.…”

Section: Introductionmentioning

confidence: 99%

Predictive prognostic value of neutrophil–lymphocytes ratio in acute coronary syndrome

Bajari

Tak

2017

Indian Heart Journal

View full text Add to dashboard Cite

show abstract

The speed of healing of myocardial infarction

Cited by 683 publications

References 5 publications

Cytosolic DNA Sensing Promotes Macrophage Transformation and Governs Myocardial Ischemic Injury

Cytosolic DNA Sensing Promotes Macrophage Transformation and Governs Myocardial Ischemic Injury

The Predictive Value of Total Neutrophil Count and Neutrophil/ Lymphocyte Ratio in Predicting In-hospital Mortality and Complications after STEMI

Predictive prognostic value of neutrophil–lymphocytes ratio in acute coronary syndrome

Contact Info

Product

Resources

About