Role of Collagen Turnover Biomarkers in the Noninvasive Assessment of Myocardial Fibrosis: An Update

Ureche, Carina; Nedelcu, Alina-Elena; Sascău, Radu Andy; Stătescu, Cristian; Kanbay, Mehmet; Covic, Adrian

doi:10.2217/bmm-2020-0298

Cited by 11 publications

(7 citation statements)

References 68 publications

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“…It has been intuitively observed that a large area of fibrotic tissue replaces normal myocardial tissue in the NP groups. This is consistent with the results of the study on myocardial fibrosis by Song et al [27], which used Masson staining. Myocardial fibrosis is an important basis for heart failure, hypertension, coronary artery disease, and other diseases [28].…”

Section: Discussionsupporting

confidence: 92%

Effects of Long-term Nonylphenol Exposure on Myocardial Fibrosis and Cardiac Function in Rats

Liu

et al. 2021

Preprint

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Background: Myocardial fibrosis is a critical pathological basis for the poor prognosis of cardiovascular diseases. Studies have found that myocardial fibrosis is closely associated with exposure to environmental estrogens such as nonylphenol (NP), as a representative of environmental estrogens. The aim of this study was to examine the effects of NP chronic exposure on myocardial fibrosis as well as cardiac structure and function. Forty Sprague Dawley rats were randomly divided into four groups (n = 10): control group (C), low NP dose (0.4 mg/kg, L), medium NP dose (4 mg/kg, M), and high NP dose (40 mg/kg, H) groups. The NP dose groups were gavaged with NP for 180 days. Results: The NP level in the heart of the NP groups was significantly higher than those in the control group (F = 43.658, P < 0.001). Serum aspartate aminotransferase (AST), creatine kinase (CK), creatine kinase isozyme (CK-MB), lactate dehydrogenase (LDH) and α-hydroxybutyrate dehydrogenase (α-HBDH) significantly increased in the NP groups compared with the control group (). Histopathological examination of the heart biopsy illustrates that in the medium and high NP groups, the fibrous connective tissue had a disordered and loose gridding shape, muscle fibers had fractured, and muscle fibers were loose with a widened gap. Extensive inflammatory cell infiltration and fibroblast proliferation in the myocardial interstitium were also found. With increasing NP dose, the degree of muscle fiber loosing and disorder became more significant in the NP treatment groups, and the collagen volume fraction (CVF) was higher than that in the control group (P < 0.01). Compared with the control group, the expression of collagen I and collagen III increased significantly in the medium and high NP groups (P < 0.05). The values of the systolic thickness of the left ventricular anterior wall (LVAWs), the diastolic thickness of the left ventricular posterior wall (LVPWd), the systolic thickness of the left ventricular posterior wall (LVPWs), and the left ventricular anterior wall (LVAWd) in the NP groups are were slightly lower than those in of the control group. The values of left ventricular end systolic dimensions (LVIDs) in the NP groups increased compared with the control group. Conclusions: Long-term NP exposure could lead to fibrosis in the rat myocardium, which is characterized by increased expressions of myocardial collagen I and collagen III, as well as elevated cardiac enzymes. In addition, the cardiac structure was affected and changes were observed in the thinner ventricular wall and as an enlarged ventricular cavity.

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Section: Discussionsupporting

confidence: 92%

Effects of Long-term Nonylphenol Exposure on Myocardial Fibrosis and Cardiac Function in Rats

Liu

et al. 2021

Preprint

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“…P3NP, a product in the metabolism of collagen type III, has prognostic value in heart failure, post-myocardial infarction can predict the incidence of AF and the recurrence after catheter ablation and the risk of ICD intervention [16]. Despite these promising studies, a recent report showed that the serum values of P3NP do not correlate with the incidence of CKD or heart failure [35].…”

Section: Discussionmentioning

confidence: 99%

“…Thus, collagen-derived biomarkers, namely PICP, P3NP, and Gal-3, that are implicated in fibrosis generating pathways, were shown to be associated with cardiac fibrosis [14,15]. Moreover, there are recent data proving that collagen-derived biomarkers are useful in several cardiac diseases and can help with the selection of patients who can benefit from anti-fibrotic interventions [16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Connection between Cardiac Fibrosis Biomarkers and Echocardiography Parameters in Advanced Chronic Kidney Disease Patients

Ureche

Dodi

Covic

et al. 2023

JCM

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Background: Myocardial fibrosis represents a mainstay pathway in the pathophysiology of uremic cardiomyopathy. This process leads to structural and functional changes in the heart, which can be detected by echocardiography. The purpose of our study was to determine the association between four echocardiographic parameters (ejection fraction (EF), global longitudinal strain (GLS), mean E/e’ ratio, and left atrial volume indexed) and biomarkers associated with cardiac fibrosis, such as procollagen type I carboxy-terminal propeptide (PICP), procollagen type III N-terminal peptide (P3NP), and galectin-3 (Gal-3) in patients with end-stage renal disease (ESRD). Methods: 140 patients with ESRD were enrolled and investigated by echocardiography and the serum levels of the aforementioned biomarkers were determined at baseline. Results: The mean EF was 53.63 ± 8%, the mean GLS was −10.2 ± 5.3%, the mean E/e’ ratio was 9.8 ± 4.3, and the mean left atrial volume indexed (LAVI) was 45.8 ± 14.2 mL/m2. The average levels for PICP, P3NP, and Gal-3 were 457.2 ± 240 µg/L, 242 ± 199.9 µg/L, and 10.7 ± 3.7 ng/mL, respectively. In regression analysis, PICP was strongly associated with all four echocardiographic parameters (EF: p = 0.0002, R2 = 0.69; GLS: p = 0.00001, R2 = 0.81; mean E/e’: p = 0.00002; R2 = 0.89; LAVI: p = 0.003; R2 = 0.73). P3NP and Gal-3 were only associated with the EF (p = 0.01, R2 = 0.31 and p = 0.02; R2 = 0.35, respectively). Conclusion: Our study evidenced that PICP, a collagen-derived biomarker, is associated with important echocardiography parameters, suggesting that it can serve as an indicator of the presence of subclinical systolic and diastolic dysfunction in patients with advanced CKD.

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“…The abnormal increase of collagen fibres could reduce the ventricular compliance and lead to the limitation of ventricular diastolic filling. If the myocardial fibrosis is further aggravated, it will inevitably damage the myocardial contractile function 45 …”

Section: Discussionmentioning

confidence: 99%

Adiponectin up‐regulates the decrease of myocardial autophagic flux induced by β₁‐adrenergic receptor autoantibody partly dependent on AMPK

Sun

Long

et al. 2021

J Cellular Molecular Medi

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Cardiomyocytes autophagy is essential for maintaining cardiac function. Our previous studies have found that β1‐adrenergic receptor autoantibody (β1‐AA) induced the decreased myocardial autophagic flux, which resulted in cardiomyocyte death and cardiac dysfunction. And other studies demonstrated that β1‐AA induced the decrease of AMPK phosphorylation, the key hub of autophagy pathway, while adiponectin up‐regulated autophagic flux mediated by AMPK. However, it is not clear whether adiponectin improves the inhibition of myocardial autophagic flux induced by β1‐AA by up‐regulating the level of AMPK phosphorylation. In this study, it has been confirmed that β1‐AA induced the decrease of AMPK phosphorylation level in both vivo and vitro. Moreover, pretreatment of cardiomyocytes with AMPK inhibitor Compound C could further reduce the autophagic flux induced by β1‐AA. Adiponectin deficiency could aggravate the decrease of myocardial AMPK phosphorylation level, autophagic flux and cardiac function induced by β1‐AA. Further, exogenous adiponectin could reverse the decline of AMPK phosphorylation level and autophagic flux induced by β1‐AA and even reduce cardiomyocyte death. While pretreated with the Compound C, the adiponectin treatment did not improve the decreased autophagosome formation, but still improved the decreased autophagosome clearance induced by β1‐AA in cardiomyocytes. This study is the first time to confirm that β1‐AA could inhibit myocardial autophagic flux by down‐regulating AMPK phosphorylation level. Adiponectin could improve the inhibition of myocardial autophagic flux induced by β1‐AA partly dependent on AMPK, so as to provide an experimental basis for the treatment of patients with β1‐AA‐positive cardiac dysfunction.

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Role of Collagen Turnover Biomarkers in the Noninvasive Assessment of Myocardial Fibrosis: An Update

Cited by 11 publications

References 68 publications

Effects of Long-term Nonylphenol Exposure on Myocardial Fibrosis and Cardiac Function in Rats

Effects of Long-term Nonylphenol Exposure on Myocardial Fibrosis and Cardiac Function in Rats

Connection between Cardiac Fibrosis Biomarkers and Echocardiography Parameters in Advanced Chronic Kidney Disease Patients

Adiponectin up‐regulates the decrease of myocardial autophagic flux induced by β₁‐adrenergic receptor autoantibody partly dependent on AMPK

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Role of Collagen Turnover Biomarkers in the Noninvasive Assessment of Myocardial Fibrosis: An Update

Cited by 11 publications

References 68 publications

Effects of Long-term Nonylphenol Exposure on Myocardial Fibrosis and Cardiac Function in Rats

Effects of Long-term Nonylphenol Exposure on Myocardial Fibrosis and Cardiac Function in Rats

Connection between Cardiac Fibrosis Biomarkers and Echocardiography Parameters in Advanced Chronic Kidney Disease Patients

Adiponectin up‐regulates the decrease of myocardial autophagic flux induced by β1‐adrenergic receptor autoantibody partly dependent on AMPK

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Product

Resources

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Adiponectin up‐regulates the decrease of myocardial autophagic flux induced by β₁‐adrenergic receptor autoantibody partly dependent on AMPK