Urinary Peptides in Heart Failure – the need for care with pees and cues

2021 ◽  
Author(s):  
A Mark Richards ◽  
C J Pemberton
Keyword(s):  
Heart Failure ◽  
Need For Care ◽  
Urinary Peptides

scholarly journals Urinary peptides in heart failure: a link to molecular pathophysiology

2021 ◽  
Author(s):  
Tianlin He ◽  
Michaela Mischak ◽  
Andrew L. Clark ◽  
Ross T. Campbell ◽  
Christian Delles ◽  
...  
Keyword(s):  
Heart Failure ◽  
Molecular Pathophysiology ◽  
Urinary Peptides

P0650URINE PEPTIDOME ANALYSIS IN HEART FAILURE, CHRONIC KIDNEY DISEASE AND CARDIORENAL SYNDROME TOWARDS THE DEFINITION OF DISEASE-SPECIFIC MARKERS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Eleni Petra ◽  
Tianlin He ◽  
Agnieszka Latosinska ◽  
Rafael Stroggilos ◽  
Harald Mischak ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Collagen Type ◽  
Cardiorenal Syndrome ◽  
Collagen Type I ◽  
Type I ◽  
Collagen Types ◽  
Alpha 1 Antitrypsin ◽  
Urinary Peptides

Abstract Background and Aims The cardiorenal syndrome (CRS) reflects the complex interplay between kidney and heart diseases, but its molecular basis remains poorly understood. Multiple studies have demonstrated the association of urinary biomarkers with both heart and kidney diseases. However, their relevance and involvement in CRS have not been investigated yet. To address this gap, a study was designed with the aim to compare urinary biomarkers specific for heart failure (HF) and chronic kidney disease (CKD) with peptides representing CRS, with the ultimate target to connect these findings towards a better understanding of CRS pathophysiology. Method A total of 3.463 urinary peptidomic datasets from patients with HF, CKD, or with both HF and CKD (CRS) as well as patients with no apparent diseases (controls) were retrieved and analyzed from the urinary peptidomics database (Latosinska A et al., Electrophoresis 2019; 40: 2294-2308). Following the matching for age, gender, heart and kidney function, differences in the abundance of urinary peptides were investigated in a cohort comprised of 390 patients with HF, 257 patients with CKD, 392 patients with CRS and 356 controls. The non-parametric Mann-Whitney U test was applied, followed by correction for multiple testing using the Benjamini-Hochberg method. To map the peptides to the protein precursor, the alignment tool Geneious (www. geneious.com) was applied, while the PeptideRanker (http://distilldeep.ucd.ie/PeptideRanker/) was used to predict probability of peptide being bioactive. Results The multiple pair-wise comparisons resulted in the identification of numerous differentially abundant peptides (p<0.05) between the studied conditions, including among others 176 HF-specific, 146 CKD-specific and 35 CRS-specific peptides. Among the HF-specific peptides, the majority (n=94, 53.4%) originated from collagen type I, II and III. In the case of CKD-specific peptides, 24 (16.43%) originated from alpha-1-antitrypsin, 19 (13.0%) from b2-microglobulin and 15 (10.27%) from collagen type I. For the CRS specific peptides, fragments of Ig lambda-2 chain C regions (n=4, 11.42%), collagen type III (n=4, 11.42%), secreted and transmembrane protein 1 (n=3, 8.57%) and gelsolin (n=1, 2.85%) were identified (figure: 1). Of the 176 HF-specific peptides, 94 (53.40%) were predicted as bioactive, including, among others, fragments of collagen types I (n=43, 45.74%) and III (n=21, 22.34%). In the former, peptides with the higher bioactivity scores were aligned close to the N terminus of the precursor protein, whereas in the latter, peptides were in close proximity to both N and C termini. Along the same lines, 32 (21.91%) of the 146 CKD-specific peptides were predicted as bioactive, including peptides from collagen types I and III with the highest score, as well as fragments from collagen type V and the C terminus of the b2-microglobulin and alpha-1-antitrypsin proteins. No CRS-specific peptides could be predicted as bioactive. Conclusion Specific urinary peptides significantly associated with CRS, but not with HF or CKD, could be identified. These data indicate that on a molecular level, CRS is not merely the result of a combination of HF and CKD, but may represent a distinct pathology, defined via specific proteomic changes. It is expected that interpretation of these findings in the context of existing literature as well as in vitro activity assays will help to understand their biological relevance in CRS.

Mitochondria in Cardiomyopathy: Alterations in Size, Number and Internal Structures

1968 ◽  
Vol 26 ◽  
pp. 126-127
Author(s):  
George Hug ◽  
William K. Schubert
Keyword(s):  
Heart Failure ◽  
Biochemical Analysis ◽  
Left Ventricular ◽  
Size Number ◽  
Internal Structures ◽  
Left Ventricular Outflow ◽  
Chest X Ray ◽  
Myocardial Fibers ◽  
Muscle Biopsies ◽  
Needle Liver Biopsy

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

Protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Galectin 3 ◽  
Consequent Increase ◽  
And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

Obstetric Applications Studied for Heart Failure Test

Ob Gyn News ◽  
2005 ◽  
Vol 40 (3) ◽  
pp. 10
Author(s):  
BRUCE JANCIN
Keyword(s):  
Heart Failure
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