Borderzone Contractile Dysfunction Is Transiently Attenuated and Left Ventricular Structural Remodeling Is Markedly Reduced Following Reperfused Myocardial Infarction in Inducible Nitric Oxide Synthase Knockout Mice

Gilson, Wesley D.; Epstein, Frederick H.; Yang, Zequan; Xu, Yaqin; Prasad, Konkal-Matt R; Toufektsian, Marie Claire; Laubach, Victor E.; French, Brent A.

doi:10.1016/j.jacc.2007.07.047

Cited by 32 publications

(35 citation statements)

References 28 publications

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“…Accordingly, previous reports showed that pharmacological inhibition or genetic inducible NO synthase deficiency in mice leads to infarct size reduction and ameliorated remodeling. [31][32][33][34] NO-dependant cytotoxicity is mediated by NOderived radicals and an inactivation of sulfur/iron-centered enzymes that are crucially involved in metabolic pathways. 35,36 Enlarged infarct size in Foxp3 DTR mice, thus, likely arises partially from a secondary loss of cardiomyocytes.…”

Section: T Reg -Cell Depletion Deteriorates Healing After MImentioning

confidence: 99%

Foxp3 ⁺ CD4 ⁺ T Cells Improve Healing After Myocardial Infarction by Modulating Monocyte/Macrophage Differentiation

Weirather

Hofmann

Beyersdorf

et al. 2014

Circulation Research

572

503

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Section: T Reg -Cell Depletion Deteriorates Healing After MImentioning

confidence: 99%

Foxp3 ⁺ CD4 ⁺ T Cells Improve Healing After Myocardial Infarction by Modulating Monocyte/Macrophage Differentiation

Weirather

Hofmann

Beyersdorf

et al. 2014

Circulation Research

572

503

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“…Thus the expression of both TNF-alpha [48] and iNOS protein [49] have been documented in cardiomyocytes bordering the infarct scar (Fig. 2).…”

Section: The Adjacent Noninfarcted Regionmentioning

confidence: 83%

“…Until such time as these novel therapies achieve a cost/benefit ratio that rivals conventional therapy, it is likely that they will be reserved for patients with larger infarcts who have more to gain from intervention. Immuno of iNOS expression in the adjacent region early and late after MI (from Gilson et al [49] with permission). Panels A&C show low-and high-power (respectively) magnifications of a wild-type (WT) mouse heart on post-myocardial infarction (MI) day 1 doubleimmunostained for myoglobin (brown) and neutrophils (purple).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of postinfarct left ventricular remodeling

French

Kramer

2007

Drug Discovery Today: Disease Mechanisms

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138

129

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Heart failure secondary to myocardial infarction (MI) remains a major source of morbidity and mortality. Long-term outcome after MI can be largely be defined in terms of its impact on the size and shape of the left ventricle (i.e., LV remodeling). Three major mechanisms contribute to LV remodeling: 1) early infarct expansion, 2) subsequent infarct extension into adjacent noninfarcted myocardium, and 3) late hypertrophy in the remote LV. Future developments in preventing post-MI heart failure will depend not only on identifying drugs targeting each of these individual mechanisms, but also on diagnostic techniques capable of assessing efficacy against each mechanism.

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“…18 One hundred fifty microliters of gadolinium-diethylenetriamine-pentaacetic acid (Gd-DTPA, 0.1 mg/kg; Magnevist, Bayer Healthcare, Germany) was injected via an indwelling intraperitoneal line, and T 1 -weighted 3-dimensional images were acquired with a flip angle of 50°.…”

Section: Late Gadolinium-enhanced Mrimentioning

confidence: 99%

Chronic Akt1 Deficiency Attenuates Adverse Remodeling and Enhances Angiogenesis After Myocardial Infarction

Vandoorne

Vandsburger

Raz

et al. 2013

Circ: Cardiovascular Imaging

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Background— Akt1 is a key signaling molecule in multiple cell types, including endothelial cells. Accordingly, Akt1 was proposed as a therapeutic target for ischemic injury in the context of myocardial infarction (MI). The aim of this study was to use multimodal in vivo imaging to investigate the impact of systemic Akt1 deficiency on cardiac function and angiogenesis before and after MI. Methods and Results— In vivo cardiac MRI was performed before and at days 1, 8, 15, and 29 to 30 after MI induction for wild-type, heterozygous, and Akt1-deficient mice. Noninfarcted hearts were imaged using ex vivo stereomicroscopy and microcomputed tomography. Histological examination was performed for noninfarcted hearts and for hearts at days 8 and 29 to 30 after MI. MRI revealed mildly decreased baseline cardiac function in Akt1 null mice, whereas ex vivo stereomicroscopy and microcomputed tomography revealed substantially reduced coronary macrovasculature. After MI, Akt1 –/– mice demonstrated significantly attenuated ventricular remodeling and a smaller decrease in ejection fraction. At 8 days after MI, a larger functional capillary network at the remote and border zone, accompanied by reduced scar extension, preserved cardiac function, and enhanced border zone wall thickening, was observed in Akt1 –/– mice when compared with littermate controls. Conclusions— Using multimodal imaging to probe the role of Akt1 in cardiac function and remodeling after MI, this study revealed reduced adverse remodeling in Akt1-deficient mice after MI. Augmented myocardial angiogenesis coupled with a more functional myocardial capillary network may facilitate revascularization and therefore be responsible for preservation of infarcted myocardium.

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Borderzone Contractile Dysfunction Is Transiently Attenuated and Left Ventricular Structural Remodeling Is Markedly Reduced Following Reperfused Myocardial Infarction in Inducible Nitric Oxide Synthase Knockout Mice

Abstract: Expression of iNOS contributes importantly to post-infarction contractile dysfunction and subsequent LV remodeling, suggesting new strategies to combat heart failure resulting from large MI.

Cited by 32 publications

References 28 publications

Foxp3 ⁺ CD4 ⁺ T Cells Improve Healing After Myocardial Infarction by Modulating Monocyte/Macrophage Differentiation

Foxp3 ⁺ CD4 ⁺ T Cells Improve Healing After Myocardial Infarction by Modulating Monocyte/Macrophage Differentiation

Mechanisms of postinfarct left ventricular remodeling

Chronic Akt1 Deficiency Attenuates Adverse Remodeling and Enhances Angiogenesis After Myocardial Infarction

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Borderzone Contractile Dysfunction Is Transiently Attenuated and Left Ventricular Structural Remodeling Is Markedly Reduced Following Reperfused Myocardial Infarction in Inducible Nitric Oxide Synthase Knockout Mice

Abstract: Expression of iNOS contributes importantly to post-infarction contractile dysfunction and subsequent LV remodeling, suggesting new strategies to combat heart failure resulting from large MI.

Cited by 32 publications

References 28 publications

Foxp3 + CD4 + T Cells Improve Healing After Myocardial Infarction by Modulating Monocyte/Macrophage Differentiation

Foxp3 + CD4 + T Cells Improve Healing After Myocardial Infarction by Modulating Monocyte/Macrophage Differentiation

Mechanisms of postinfarct left ventricular remodeling

Chronic Akt1 Deficiency Attenuates Adverse Remodeling and Enhances Angiogenesis After Myocardial Infarction

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Resources

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Foxp3 ⁺ CD4 ⁺ T Cells Improve Healing After Myocardial Infarction by Modulating Monocyte/Macrophage Differentiation

Foxp3 ⁺ CD4 ⁺ T Cells Improve Healing After Myocardial Infarction by Modulating Monocyte/Macrophage Differentiation