Cardiac biomarkers of heart failure in chronic kidney disease

Han, Xiao; Zhang, Shuai; Chen, Zhongbo; Adhikari, Binay Kumar; Zhang, Ying; Zhang, Jin; Sun, Jian; Wang, Yonggang

doi:10.1016/j.cca.2020.07.040

Cited by 63 publications

(58 citation statements)

References 173 publications

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“…Galectin-3 can regulate numerous biological processes, such as pre-mRNA splicing, cell growth, apoptosis, differentiation, transformation, angiogenesis, inflammation, fibrosis, and host defense [12]. Galectin-3 also plays a vital role as a diagnostic, and prognostic biomarker, or a therapeutic target for cardiovascular diseases, chronic kidney diseases, autoimmune and nonautoimmune nephropathies, fatty liver, viral infection, autoimmune diseases, neurodegenerative disorders, and tumor formation [21,[27][28][29][30][31]. Galectin-3 can be secreted extracellularly but also can shuttle into the nucleus.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Mesenchymal stem cells ameliorate renal fibrosis by galectin-3/Akt/GSK3β/Snail signaling pathway in adenine-induced nephropathy rat

et al. 2021

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Background Tubulointerstitial fibrosis (TIF) is one of the main pathological features of various progressive renal damages and chronic kidney diseases. Mesenchymal stromal cells (MSCs) have been verified with significant improvement in the therapy of fibrosis diseases, but the mechanism is still unclear. We attempted to explore the new mechanism and therapeutic target of MSCs against renal fibrosis based on renal proteomics. Methods TIF model was induced by adenine gavage. Bone marrow-derived MSCs was injected by tail vein after modeling. Renal function and fibrosis related parameters were assessed by Masson, Sirius red, immunohistochemistry, and western blot. Renal proteomics was analyzed using iTRAQ-based mass spectrometry. Further possible mechanism was explored by transfected galectin-3 gene for knockdown (Gal-3 KD) and overexpression (Gal-3 OE) in HK-2 cells with lentiviral vector. Results MSCs treatment clearly decreased the expression of α-SMA, collagen type I, II, III, TGF-β1, Kim-1, p-Smad2/3, IL-6, IL-1β, and TNFα compared with model rats, while p38 MAPK increased. Proteomics showed that only 40 proteins exhibited significant differences (30 upregulated, 10 downregulated) compared MSCs group with the model group. Galectin-3 was downregulated significantly in renal tissues and TGF-β1-induced rat tubular epithelial cells and interstitial fibroblasts, consistent with the iTRAQ results. Gal-3 KD notably inhibited the expression of p-Akt, p-GSK3β and snail in TGF-β1-induced HK-2 cells fibrosis. On the contrary, Gal-3 OE obviously increased the expression of p-Akt, p-GSK3β and snail. Conclusion The mechanism of MSCs anti-renal fibrosis was probably mediated by galectin-3/Akt/GSK3β/Snail signaling pathway. Galectin-3 may be a valuable target for treating renal fibrosis.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Mesenchymal stem cells ameliorate renal fibrosis by galectin-3/Akt/GSK3β/Snail signaling pathway in adenine-induced nephropathy rat

et al. 2021

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“…Unfortunately, natriuretic peptide levels are increased in patients with low eGFR independently of the presence of HF. A recent review highlighted the different biomarkers that can be used for HF prognosis in patients with chronic kidney disease, indicating that Gal-3 could be more useful than NT-proBNP being less influenced by eGFR [131]. In patients with chronic kidney disease without signs of HF at recruitment, high Gal-3 levels were associated with early symptomatic changes of HF, although with a hazard ratio lower than that of growth differentiation factor-15 (GDF-15) [132].…”

Section: Heart Failurementioning

confidence: 99%

Galectin-3 in Cardiovascular Diseases

Blanda

Bracale

Taranto

et al. 2020

IJMS

127

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Galectin-3 (Gal-3) is a β-galactoside-binding protein belonging to the lectin family with pleiotropic regulatory activities and several physiological cellular functions, such as cellular growth, proliferation, apoptosis, differentiation, cellular adhesion, and tissue repair. Inflammation, tissue fibrosis and angiogenesis are the main processes in which Gal-3 is involved. It is implicated in the pathogenesis of several diseases, including organ fibrosis, chronic inflammation, cancer, atherosclerosis and other cardiovascular diseases (CVDs). This review aims to explore the connections of Gal-3 with cardiovascular diseases since they represent a major cause of morbidity and mortality. We herein discuss the evidence on the pro-inflammatory role of Gal-3 in the atherogenic process as well as the association with plaque features linked to lesion stability. We report the biological role and molecular mechanisms of Gal-3 in other CVDs, highlighting its involvement in the development of cardiac fibrosis and impaired myocardium remodelling, resulting in heart failure and atrial fibrillation. The role of Gal-3 as a prognostic marker of heart failure is described together with possible diagnostic applications to other CVDs. Finally, we report the tentative use of Gal-3 inhibition as a therapeutic approach to prevent cardiac inflammation and fibrosis.

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“…In this context, the decrease of renal clearance and the cardiac stress impacts biomarker levels [34]. This diagnostic limitation is moderate in patients with preserved renal function (estimated glomerular filtration rate (eGFR) >60 mL•min −1 •m −2 ) whereas adapted cut-off values have to be used in patients with chronic renal failure [34]. In our cohort, the majority of patients had preserved renal function or slightly reduced eGFR at baseline.…”

Section: Key Findingsmentioning

confidence: 93%

“…Chronic renal failure frequently occurs as one negative side effect of pulmonary hypertension and right heart failure [32,33]. In this context, the decrease of renal clearance and the cardiac stress impacts biomarker levels [34]. This diagnostic limitation is moderate in patients with preserved renal function (estimated glomerular filtration rate (eGFR) >60 mL•min −1 •m −2 ) whereas adapted cut-off values have to be used in patients with chronic renal failure [34].…”

Section: Key Findingsmentioning

confidence: 99%

Mid-regional pro-atrial natriuretic peptide and copeptin as indicators of disease severity and therapy response in CTEPH

et al. 2020

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BackgroundChronic thromboembolic pulmonary hypertension (CTEPH) leads to right heart failure. Pulmonary endarterectomy (PEA) or balloon pulmonary angioplasty (BPA) restore pulmonary haemodynamics and allow cardiac recovery. This study examined the relationship of copeptin and mid-regional pro-atrial natriuretic peptide (MR-proANP) levels to disease severity and therapy response.MethodsThis observational cohort study included 125 patients (55 PEA/70 BPA) who underwent treatment and completed a 6-/12-month follow-up. Biomarkers, measured at baseline, prior to every BPA and at follow-up, were compared to 1) severe disease at baseline (right atrial pressure (RAP) ≥8 mmHg and cardiac index ≤2.4 L·min−1·m−2) and 2) optimal therapy response (no persistent pulmonary hypertension combined with a normalised RAP (mean PAP ≤25 mmHg, pulmonary vascular resistance (PVR) ≤3 WU and RAP ≤6 mmHg) or a reduction in mean PAP ≥25%, PVR ≥35% and RAP ≥25%).ResultsSeverely diseased patients had higher levels of MR-proANP (320 (246–527) pmol·L−1versus 133 (82–215) pmol·L−1; p=0.001) and copeptin (12.7 (7.3–20.6) pmol·L−1versus 6.8 (4.4–12.8) pmol·L−1; p=0.015) at baseline than the rest of the cohort. At baseline, MR-proANP (area under the curve (AUC) 0.91; cut-off value 227 pmol·L−1; OR 56, 95% CI 6.9–454.3) and copeptin (AUC 0.70; cut-off value 10.9 pmol·L−1; OR 1.5, 95% CI 1.2–1.9) identified severely diseased patients. After PEA/BPA, levels of MR-proANP (99 (58–145) pmol·L−1; p<0.001) and copeptin (6.3 (3.7–12.6) pmol·L−1; p=0.009) decreased and indicated optimal therapy response (MR-proANP <123 pmol·L−1 (AUC 0.70) and copeptin <10.1 pmol·L−1 (AUC 0.58)).ConclusionMR-proANP and copeptin levels are affected in CTEPH and decrease after therapy. MR-proANP identifies a severe disease status and optimal therapy response.

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Cardiac biomarkers of heart failure in chronic kidney disease

Cited by 63 publications

References 173 publications

RETRACTED ARTICLE: Mesenchymal stem cells ameliorate renal fibrosis by galectin-3/Akt/GSK3β/Snail signaling pathway in adenine-induced nephropathy rat

RETRACTED ARTICLE: Mesenchymal stem cells ameliorate renal fibrosis by galectin-3/Akt/GSK3β/Snail signaling pathway in adenine-induced nephropathy rat

Galectin-3 in Cardiovascular Diseases

Mid-regional pro-atrial natriuretic peptide and copeptin as indicators of disease severity and therapy response in CTEPH

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