Multiplicity of Nitric Oxide and Natriuretic Peptide Signaling in Heart Failure

Preedy, Michael E. J.; Baliga, Reshma S.; Hobbs, Adrian J.

doi:10.1097/fjc.0000000000000724

Cited by 19 publications

(22 citation statements)

References 322 publications

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“…Whereas NO/cGMP-induced vasorelaxation as prototypical biological NO response has been known for decades, the protective role of NO-induced cGMP in cardiovascular events such as cardiovascular remodeling and fibrosis is a matter of current research [1,3]. A possible role of NO-dependent cGMP in fibrosis development is further underlined by the finding of comparably high NO-induced cGMP signals in cardiac fibroblasts and their recently described absence in cardiac myocytes [9].…”

Section: Discussionmentioning

confidence: 99%

“…cGMP is an important second messenger in the cardiovascular system and plays a crucial role in the regulation of smooth muscle tone. In addition, cGMP has been proposed to inhibit smooth muscle proliferation and to exert protective effects against cardiovascular remodeling and fibrosis [1][2][3]. Within the NO/cGMP pathway, the cGMP-forming, NO-sensitive guanylyl cyclase (NO-GC) acts as NO receptor.…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin II-Induced Cardiovascular Fibrosis Is Attenuated by NO-Sensitive Guanylyl Cyclase1

Broekmans

Giesen

Menges

et al. 2020

Cells

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In the NO/cGMP signaling cascade, relevant in the cardiovascular system, two NO-sensitive guanylyl cyclase (NO-GC) isoforms are responsible for NO-dependent cGMP generation. Here, the impact of the major NO-GC isoform, NO-GC1, on fibrosis development in the cardiovascular system was studied in NO-GC1-deficient mice treated with AngiotensinII (AngII), known to induce vascular and cardiac remodeling. Morphometric analysis of NO-GC1 KO’s aortae demonstrated an enhanced increase of perivascular area after AngII treatment accompanied by a higher aortic collagen1 mRNA content. Increased perivascular fibrosis also occurred in cardiac vessels of AngII-treated NO-GC1 KO mice. In line, AngII-induced interstitial fibrosis was 32% more pronounced in NO-GC1 KO than in WT myocardia associated with a higher cardiac Col1 and other fibrotic marker protein content. In sum, increased perivascular and cardiac interstitial fibrosis together with the enhanced collagen1 mRNA content in AngII-treated NO-GC1-deficient mice represent an exciting manifestation of antifibrotic properties of cGMP formed by NO-GC1, a finding with great pharmaco-therapeutic implications.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Angiotensin II-Induced Cardiovascular Fibrosis Is Attenuated by NO-Sensitive Guanylyl Cyclase1

Broekmans

Giesen

Menges

et al. 2020

Cells

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“…Here, we first proved that β1AA, which were extracted from the postpartum rats with autoimmunity, directly induce apoptosis in H9C2 cardiac myocytes through β1AR. It signifies that apoptosis plays a pathophysiological role in heart failure [27]. Thus, these results suggest that β1AA may directly contribute to the pathogenesis of PPCM.…”

Section: Discussionmentioning

confidence: 61%

β1 adrenoceptor antibodies induce myocardial apoptosis via inhibiting PGC-1α-related pathway

Shi

Liu

Zhang

et al. 2020

BMC Cardiovasc Disord

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Background: Peripartum cardiomyopathy (PPCM) is life-threatening heart disease. However, the causes and pathogenesis of PPCM remain unclear. Previous studies found that β1 adrenoceptor antibodies (β1AA) had possible involvement in the development of PPCM. In the present study, we determined the potential relationship between PPCM and β1AA, including the mechanism of β1AA leading to PPCM. Methods: We extracted the β1AA from the postpartum Wistar rats that were injected by the antigen peptide segment of the β1 adrenoceptor to produce PPCM. We tested the effects of β1AA on H9C2 cell line by CCK-8, LDH, TUNEL, SA-ELISA, qRT-PCR, and western blot methods. Furthermore, PGC-1α was overexpressed to rescue the effect of β1AA on H9C2 cells. Results: We found that the extracted β1AA induced apoptosis of cardiac myocytes of H9C2 cell line. Moreover, the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), which is a master regulator of mitochondrial metabolism, and its downstream transcript vascular endothelial growth factor (VEGF) got decreased in H9C2 cells after β1AA treatment. In addition, the effect of β1AA could be inhibited by atenolol, the antagonist of β1 adrenoceptors (β1AR) and imitated by isoprenaline, the agonist of β1AR. Furthermore, overexpression of PGC-1α in the H9C2 cells rescued the apoptosis of cells and inhibitory expression of VEGF induced by β1AA. Conclusions: Our results suggest that the symptoms of PPCM due to myocardial cell apoptosis induced by β1AA inhibiting the PGC-1α-related pathway impairs mitochondrial energy metabolism. Therefore, our results uncover a previously unknown role of the β1AA pathway in the etiology of PPCM and provide a novel potential target for the treatment of PPCM.

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“…Increased levels of cGMP in cirrhotic ventricles and elevated serum and cardiac levels of cytokines such as TNF‐α suggest a cytokine/NO/cGMP pathway for this effect 118 . Effects of NO on cardiac function in pathophysiological states have been extensively reviewed previously 121,122 …”

Section: Pathogenic Mechanismsmentioning

confidence: 99%

Review article: comprehensive analysis of cirrhotic cardiomyopathy

Chahal

Liu

Shamatutu

et al. 2021

Aliment Pharmacol Ther

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SummaryBackgroundPatients with cirrhosis are at risk of developing cirrhotic cardiomyopathy. This syndrome is unique to cirrhosis and is generally defined as subnormal cardiac function in the absence of prior heart disease. There is no systematic or comprehensive review of cirrhotic cardiomyopathy to date.AimsTo comprehensively review the literature on the definition, pathogenic mechanisms, diagnostic criteria, prevalence, management and influence on liver transplantation including reversibility of cirrhotic cardiomyopathy.MethodsElectronic searches of the EMBASE, MEDLINE, EBM Reviews—Cochrane Central Register of Controlled Trials, EBM Reviews—Cochrane Database of Systematic Reviews and Google Scholar databases were conducted. MeSH terms focused on cirrhosis, cardiomyopathy, medication classes and epidemiology. Literature up to August 2020 was reviewed.ResultsNew diagnostic criteria for the definition of cirrhotic cardiomyopathy have recently been published, consisting of systolic and diastolic dysfunction parameters as assessed by echocardiographic methods. The roles of electrocardiographic disturbances and biomarkers in the definition criteria remain unclear. Pathogenic mechanisms underlying cirrhotic cardiomyopathy are likely related to the inflammatory phenotype of cirrhosis. Prevalence rates of 26%‐81% in cirrhotic patients are reported. Several medical therapies have been proposed, but none with clear evidence of efficacy. The presence of cirrhotic cardiomyopathy complicates the liver transplantation process with a higher risk of adverse cardiovascular events post‐transplant. Complete reversibility of the syndrome after transplantation remains controversial but most studies suggest that it does not occur at least within the first post‐operative year.ConclusionsCirrhotic cardiomyopathy is a clinically relevant syndrome that affects morbidity and mortality in patients with cirrhosis.

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Multiplicity of Nitric Oxide and Natriuretic Peptide Signaling in Heart Failure

Cited by 19 publications

References 322 publications

Angiotensin II-Induced Cardiovascular Fibrosis Is Attenuated by NO-Sensitive Guanylyl Cyclase1

Angiotensin II-Induced Cardiovascular Fibrosis Is Attenuated by NO-Sensitive Guanylyl Cyclase1

β1 adrenoceptor antibodies induce myocardial apoptosis via inhibiting PGC-1α-related pathway

Review article: comprehensive analysis of cirrhotic cardiomyopathy

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