Letter by Campbell Regarding Article, “Coronary Microvascular Rarefaction and Myocardial Fibrosis in Heart Failure With Preserved Ejection Fraction”

Campbell, Duncan J.

doi:10.1161/circulationaha.115.016091

Cited by 3 publications

(4 citation statements)

References 6 publications

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“…New myocardium requires concomitant establishment of adequate vascular supply, 16 as appropriate coronary vascularity is critical for life‐long function and health 17‐21 . Inadequate coronary supply contributes to angina, cardiac syndrome X, impaired cardiac function, impaired healing, and cellular necrosis and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

“…New myocardium requires concomitant establishment of adequate vascular supply, 16 as appropriate coronary vascularity is critical for life-long function and health. [17][18][19][20][21] Inadequate coronary supply contributes to angina, cardiac syndrome X, impaired cardiac function, impaired healing, and cellular necrosis and apoptosis. Although regulation of vascular growth is a very complex process, IGF-1 is a good candidate for initiating coronary growth in the fetus as it stimulates endothelial and vascular smooth muscle growth and regulates vascular function in other models.…”

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confidence: 99%

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Coronary vascular growth matches IGF‐1‐stimulated cardiac growth in fetal sheep

et al. 2020

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Heart disease is the leading cause of death in the United States despite advanced medical and interventional therapies. 1 The push to develop regenerative therapies for the adult myocardium has so far been unsuccessful because cardiac myocytes are nonproliferative after the perinatal period, and establishing a differentiated electrical syncytium from stem cells with necessary interstitial and vascular cells and structures has proved challenging. 2 Young age has been found to be key to stimulating abundant, healthy proliferation of working cardiac myocytes and expansion of the coronary vasculature, 3-10 therefore, therapies to stimulate therapeutic myocardial expansion might first be successful in fetuses

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

Coronary vascular growth matches IGF‐1‐stimulated cardiac growth in fetal sheep

et al. 2020

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“…These data suggest that the cardiac vascular network may be compromised, but the progression toward heart failure, with a significant~40% reduction in ejection fraction, is not compounded by LINC00961 -/-. It has previously been reported that reduced coronary vascularity increases cardiac vulnerability to fibrosis [35][36][37]. Reduced blood flow to the functional myocardium compromises coronary flow reserve required during increased cardiovascular work and pathological conditions [30,38].…”

Section: Discussionmentioning

confidence: 99%

The Influence of the LINC00961/SPAAR Locus Loss on Murine Development, Myocardial Dynamics, and Cardiac Response to Myocardial Infarction

Spiroski

Sanders

Meloni

et al. 2021

IJMS

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Long non-coding RNAs (lncRNAs) have structural and functional roles in development and disease. We have previously shown that the LINC00961/SPAAR (small regulatory polypeptide of amino acid response) locus regulates endothelial cell function, and that both the lncRNA and micropeptide counter-regulate angiogenesis. To assess human cardiac cell SPAAR expression, we mined a publicly available scRNSeq dataset and confirmed LINC00961 locus expression and hypoxic response in a murine endothelial cell line. We investigated post-natal growth and development, basal cardiac function, the cardiac functional response, and tissue-specific response to myocardial infarction. To investigate the influence of the LINC00961/SPAAR locus on longitudinal growth, cardiac function, and response to myocardial infarction, we used a novel CRISPR/Cas9 locus knockout mouse line. Data mining suggested that SPAAR is predominantly expressed in human cardiac endothelial cells and fibroblasts, while murine LINC00961 expression is hypoxia-responsive in mouse endothelial cells. LINC00961–/– mice displayed a sex-specific delay in longitudinal growth and development, smaller left ventricular systolic and diastolic areas and volumes, and greater risk area following myocardial infarction compared with wildtype littermates. These data suggest the LINC00961/SPAAR locus contributes to cardiac endothelial cell and fibroblast function and hypoxic response, growth and development, and basal cardiovascular function in adulthood.

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“…It has previously been reported that reduced coronary vascularity increases cardiac vulnerability to fibrosis. [35][36][37] Reduced blood flow to the functional myocardium compromises coronary flow reserve required during increased cardiovascular work and pathological conditions. [30,38] Future investigations on the microvascular network during the acute remodelling window post-MI will help identify the contribution of LINC00961 and SPAAR to extracellular matrix remodelling and the secretion of matrix metalloproteinases, fibronectin, and proteoglycans during cardiac scar maturation.…”

Section: Discussionmentioning

confidence: 99%

The Influence of the LINC00961/SPAAR Locus Loss on Murine Development, Myocardial Dynamics, and Cardiac Response to Myocardial Infarction

Spiroski

Sanders

Meloni

et al. 2020

Preprint

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Long non-coding RNAs (lncRNAs) have structural and functional roles in development and disease. We have previously shown that the LINC00961/SPAAR locus regulates endothelial cell function, and that both the lncRNA and micropeptide counter-regulate angiogenesis. To assess human cardiac cell SPAAR expression we mined a publicly available scRNSeq dataset and confirmed LINC00961 locus expression and hypoxic response in a murine endothelial cell line. We investigated post-natal growth and development, basal cardiac function, the cardiac functional response and tissue-specific response to myocardial infarction. To investigate the contribution of the LINC00961/SPAAR locus to determination of longitudinal growth, cardiac function, and response to myocardial infarction, we used a novel CRISPR/Cas9 locus knockout mouse line. Data mining suggested that SPAAR is predominantly expressed in human cardiac endothelial cells and fibroblasts, while murine LINC00961 expression is hypoxia-responsive in mouse endothelial cells. LINC00961-/- mice displayed a sex-specific delay in longitudinal growth and development, smaller left ventricular systolic and diastolic areas and volumes, and greater risk area following myocardial infarction compared with wildtype littermates. These data suggest a role for the LINC00961/SPAAR locus in cardiac endothelial cell and fibroblast cell function and hypoxic-response, and in growth and development, and basal cardiovascular function in adulthood.

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Letter by Campbell Regarding Article, “Coronary Microvascular Rarefaction and Myocardial Fibrosis in Heart Failure With Preserved Ejection Fraction”

Cited by 3 publications

References 6 publications

Coronary vascular growth matches IGF‐1‐stimulated cardiac growth in fetal sheep

Coronary vascular growth matches IGF‐1‐stimulated cardiac growth in fetal sheep

The Influence of the LINC00961/SPAAR Locus Loss on Murine Development, Myocardial Dynamics, and Cardiac Response to Myocardial Infarction

The Influence of the LINC00961/SPAAR Locus Loss on Murine Development, Myocardial Dynamics, and Cardiac Response to Myocardial Infarction

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