Insulin-like growth factor binding protein-2: a new circulating indicator of pulmonary arterial hypertension severity and survival

Yang, Jun; Griffiths, Megan; Nies, Melanie; Brandal, Stephanie; Damico, Rachel; Vaidya, Dhananjay; Tao, Xuguang Grant; Simpson, Carol; Kolb, Todd M.; Mathai, Stephen C.; Pauciulo, Michael W.; Nichols, William C.; Ivy, D. Dunbar; Austin, Eric D.; Hassoun, Paul M.

doi:10.1186/s12916-020-01734-3

Cited by 22 publications

(33 citation statements)

References 44 publications

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“…The excessive release of growth factors (IGF-BP2 in this case) during lung remodeling processes in the setting of post-capillary PH is also not surprising. Yang et al [32] found markedly increased plasma concentrations of IGF-BP2 in two independent pulmonary artery hypertension (PAH) collectives. In conclusion, the levels of su-PAR measured here could also be consistent with current literature.…”

Section: Discussionmentioning

confidence: 99%

Systolic Pulmonary Artery Pressure and Cardiovascular Biomarkers—New Non-Invasive Ways to Detect Pulmonary Hypertension in Patients with Severe Aortic Valve Stenosis Undergoing TAVR?

Boxhammer¹,

Köller²,

Paar³

et al. 2022

Rev. Cardiovasc. Med.

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Background: Patients with severe aortic valve stenosis (AS) frequently present with pulmonary hypertension (PH). The gold standard for detection of pulmonary hypertension is right heart catheterization, which is not routinely performed as a preoperative standard in cardiology centers today, neither before surgical valve replacement nor before transcatheter aortic valve replacement (TAVR) procedure. Echocardiographic determination of systolic pulmonary artery pressure (sPAP) provides an opportunity to assess the presence or absence of PH. The aim of the present study was to investigate the extent to which plasma levels of common cardiovascular biomarkers behave in patients with severe AS and an sPAP <40 mmHg in comparison to patients with an sPAP ≥40 mmHg. Methods: 179 patients with echocardiographic evidence of severe AS before TAVR procedure were divided into 2 groups based on sPAP. An sPAP of 40 mmHg was considered the cut-off value, with absence of PH defined by an sPAP <40 mmHg (n = 82) and presence of PH defined by an sPAP ≥40 mmHg (n = 97). Directly before TAVR, a blood sample was drawn from each patient, and plasma concentrations of the cardiovascular biomarkers Soluble Suppression of Tumorigenicity-2 (sST2), Growth/Differentiation of Factor-15 (GDF-15), Heart-Type Fatty-Acid Binding Protein (H-FABP), Insulin Like Growth Factor Binding Protein 2 (IGF-BP2), Soluble Urokinase-Type Plasminogen Activator Receptor (suPAR), Brain Natriuretic Peptide (BNP) and Cardiac Troponin I (cTnI) were determined. Results: Patients with an sPAP ≥40 mmHg had significantly higher sST2 (p = 0.010), GDF-15 (p = 0.005), IGF-BP2 (p = 0.029), suPAR (p = 0.018), BNP (p < 0.001) and cTnI (p = 0.039) plasma levels. Only for H-FABP (p = 0.069), no significant differences were discernible between the two groups. In addition, cut-off values were calculated to predict an sPAP ≥40 mmHg. Significant results were shown with 16045.84 pg/mL for sST2 (p = 0.010), with 1117.54 pg/mL for GDF-15 (p = 0.005), with 107028.43 pg/mL for IGF-BP2 (p = 0.029), with 3782.84 pg/mL for suPAR (p = 0.018), with 2248.00 pg/mL for BNP (p < 0.001) and with 20.50 pg/mL for cTnI (p = 0.002). Conclusions: sPAP as an echocardiographic parameter in combination with supplementary use of cardiovascular biomarkers presented here have the potential to provide more detailed information about the presence or absence of PH in a non-invasive way.

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Section: Discussionmentioning

confidence: 99%

Systolic Pulmonary Artery Pressure and Cardiovascular Biomarkers—New Non-Invasive Ways to Detect Pulmonary Hypertension in Patients with Severe Aortic Valve Stenosis Undergoing TAVR?

Boxhammer¹,

Köller²,

Paar³

et al. 2022

Rev. Cardiovasc. Med.

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“…For example, NT-proBNP in the urine of preterm infants has been shown to inform about pulmonary hypertension (Naeem et al 2020 ). IGFBP-2 is an indicator of pulmonary arterial hypertension (PAH) (Yang et al 2020 ) and can predict a decline of kidney function in type 2 diabetes (Narayanan et al 2012 ). FABP4 has been implicated in proteinuria and has been discussed as a marker of kidney glomerular damage (Okazaki 2014 ).…”

Section: Resultsmentioning

confidence: 99%

Urine-based multi-omic comparative analysis of COVID-19 and bacterial sepsis-induced ARDS

Batra

Uni²,

Akchurin

et al. 2023

Mol Med

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Background Acute respiratory distress syndrome (ARDS), a life-threatening condition during critical illness, is a common complication of COVID-19. It can originate from various disease etiologies, including severe infections, major injury, or inhalation of irritants. ARDS poses substantial clinical challenges due to a lack of etiology-specific therapies, multisystem involvement, and heterogeneous, poor patient outcomes. A molecular comparison of ARDS groups holds the potential to reveal common and distinct mechanisms underlying ARDS pathogenesis. Methods We performed a comparative analysis of urine-based metabolomics and proteomics profiles from COVID-19 ARDS patients (n = 42) and bacterial sepsis-induced ARDS patients (n = 17). To this end, we used two different approaches, first we compared the molecular omics profiles between ARDS groups, and second, we correlated clinical manifestations within each group with the omics profiles. Results The comparison of the two ARDS etiologies identified 150 metabolites and 70 proteins that were differentially abundant between the two groups. Based on these findings, we interrogated the interplay of cell adhesion/extracellular matrix molecules, inflammation, and mitochondrial dysfunction in ARDS pathogenesis through a multi-omic network approach. Moreover, we identified a proteomic signature associated with mortality in COVID-19 ARDS patients, which contained several proteins that had previously been implicated in clinical manifestations frequently linked with ARDS pathogenesis. Conclusion In summary, our results provide evidence for significant molecular differences in ARDS patients from different etiologies and a potential synergy of extracellular matrix molecules, inflammation, and mitochondrial dysfunction in ARDS pathogenesis. The proteomic mortality signature should be further investigated in future studies to develop prediction models for COVID-19 patient outcomes.

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“…For example, NT-proBNP in the urine of preterm infants has been shown to inform about pulmonary hypertension 40 . IGFBP-2 is an indicator of pulmonary arterial hypertension (PAH) 41 and can predict a decline of kidney function in type 2 diabetes 42 . FABP4 has been implicated in proteinuria and has been discussed as a marker of kidney glomerular damage 43 .…”

Section: Ards-specific Heterogeneity Of Molecular Associations Across...mentioning

confidence: 99%

Urine-based multi-omic comparative analysis of COVID-19 and bacterial sepsis-induced ARDS

Batra

Uni²,

Akchurin

et al. 2022

Preprint

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Acute respiratory distress syndrome (ARDS), a life-threatening condition during critical illness, is a common complication of COVID-19. It can originate from various disease etiologies, including severe infections, major injury, or inhalation of irritants. ARDS poses substantial clinical challenges due to a lack of etiology-specific therapies, multisystem involvement, and heterogeneous, poor patient outcomes. A molecular comparison of ARDS groups holds the potential to reveal common and distinct mechanisms underlying ARDS pathogenesis. In this study, we performed a comparative analysis of urine-based metabolomics and proteomics profiles from COVID-19 ARDS patients (n = 42) and bacterial sepsis-induced ARDS patients (n = 17). The comparison of these ARDS etiologies identified 150 metabolites and 70 proteins that were differentially abundant between the two groups. Based on these findings, we interrogated the interplay of cell adhesion/extracellular matrix molecules, inflammation, and mitochondrial dysfunction in ARDS pathogenesis through a multi-omic network approach. Moreover, we identified a proteomic signature associated with mortality in COVID-19 ARDS patients, which contained several proteins that had previously been implicated in clinical manifestations frequently linked with ARDS pathogenesis. In summary, our results provide evidence for significant molecular differences in ARDS patients from different etiologies and a potential synergy of extracellular matrix molecules, inflammation, and mitochondrial dysfunction in ARDS pathogenesis. The proteomic mortality signature should be further investigated in future studies to develop prediction models for COVID-19 patient outcomes.

show abstract

Insulin-like growth factor binding protein-2: a new circulating indicator of pulmonary arterial hypertension severity and survival

Cited by 22 publications

References 44 publications

Systolic Pulmonary Artery Pressure and Cardiovascular Biomarkers—New Non-Invasive Ways to Detect Pulmonary Hypertension in Patients with Severe Aortic Valve Stenosis Undergoing TAVR?

Systolic Pulmonary Artery Pressure and Cardiovascular Biomarkers—New Non-Invasive Ways to Detect Pulmonary Hypertension in Patients with Severe Aortic Valve Stenosis Undergoing TAVR?

Urine-based multi-omic comparative analysis of COVID-19 and bacterial sepsis-induced ARDS

Urine-based multi-omic comparative analysis of COVID-19 and bacterial sepsis-induced ARDS

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