Differential protein profiling as a potential multi-marker approach for obese patients with heart failure: A retrospective study

Timotin, Andreï; Cinato, Mathieu; Boal, Frédéric; Déjean, Sébastien; Anesia, Rodica; Arnaut, Oleg; Lagente, Christine; Roncalli, Jérôme; Desmoulin, Franck; Kunduzova, Oksana

doi:10.1038/s41598-018-26118-9

Cited by 5 publications

(12 citation statements)

References 22 publications

(22 reference statements)

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“…The notion of MMP1/PAR1 axis was initially demonstrated in the process of infection [ 41 ]. Later, emerging evidence indicated that MMP1/PAR1 axis participated in the pathogenesis of thrombosis [ 42 ], atherosclerosis [ 43 ], and serious cardiac events [ 44 ]. Recent studies support a critical role of MMP1/PAR1 axis in tumor development and progression.…”

Section: Discussionmentioning

confidence: 99%

Tumor-associated macrophages (TAMs) depend on MMP1 for their cancer-promoting role

Guo

et al. 2021

Cell Death Discov.

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The complex interaction between tumor-associated macrophages (TAMs) and tumor cells through several soluble factors and signaling is essential for colorectal cancer (CRC) progression. However, the molecular mechanism involved remains elusive. In this study, we demonstrated that MMP1 derived from TAMs markedly facilitated colon cancer cell proliferation via accelerating cell cycle transition from G0/G1 to S and G2/M phase. Moreover, exogenous MMP1 activated cdc25a/CDK4-cyclin D1 and p21/cdc2-cyclin B1 complexes through altering c-Myc and ETV4. Mechanistic studies indicated that inhibition of PAR1 or blockage of MAPK/Erk signaling eliminated the proliferation induced by exogenous MMP1 in vitro and in vivo. In addition, ETV4 could bind to the promoter of MMP1 and activate MMP1 transcription, which confirmed the MMP1/ETV4/MMP1 positive feedback. Altogether, our study identified a cytokine paracrine manner between colon cancer cells and TAMs. MMP1/PAR1/Erk1/2/ETV4 positive feedback loop may represent to be a therapeutic target and prognostic marker in CRC.

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Section: Discussionmentioning

confidence: 99%

Tumor-associated macrophages (TAMs) depend on MMP1 for their cancer-promoting role

Guo

et al. 2021

Cell Death Discov.

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“…The association between MMP9 and worsening events in chronic HF patients has been described 35 , but there are only few papers about the 2 MMPs identified here. A recent study has shown that MMP1 with protease-activated receptors (PAR) 1 and BNP and NTproBNP were downregulated in obese HF patients 36 . Interestingly, mechanistic research showed that inflammation mediated by MMP1-PAR1 might amplify tumour necrosis factor α signalling in endothelial cells 37 .…”

Section: Discussionmentioning

confidence: 99%

Circulating proteomic signature of early death in heart failure patients with reduced ejection fraction

Cuvelliez

Vandewalle

Brunin

et al. 2019

Sci Rep

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Heart failure (HF) remains a main cause of mortality worldwide. Risk stratification of patients with systolic chronic HF is critical to identify those who may benefit from advanced HF therapies. The aim of this study is to identify plasmatic proteins that could predict the early death (within 3 years) of HF patients with reduced ejection fraction hospitalized in CHRU de Lille. The subproteome targeted by an aptamer-based technology, the Slow Off-rate Modified Aptamer (SOMA) scan assay of 1310 proteins, was profiled in blood samples from 168 HF patients, and 203 proteins were significantly modulated between patients who died of cardiovascular death and patients who were alive after 3 years of HF evaluation (Wilcoxon test, FDR 5%). A molecular network was built using these 203 proteins, and the resulting network contained 2281 molecules assigned to 34 clusters annotated to biological pathways by Gene Ontology. This network model highlighted extracellular matrix organization as the main mechanism involved in early death in HF patients. In parallel, an adaptive Least Absolute Shrinkage and Selection Operator (LASSO) was performed on these 203 proteins, and six proteins were selected as candidates to predict early death in HF patients: complement C3, cathepsin S and F107B were decreased and MAPK5, MMP1 and MMP7 increased in patients who died of cardiovascular causes compared with patients living 3 years after HF evaluation. This proteomic signature of 6 circulating plasma proteins allows the identification of systolic HF patients with a risk of early death.

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“…113 In patients with heart failure, obesity is associated with increased leptin plasma level, whereas the VEGF A plasma level is decreased. 114 Overweight patients with CAD have higher leptin and VEGF blood concentration than overweight controls without CAD, and atorvastatin treatment decreases both leptin and VEGF serum level in CAD subjects. 115 In older adults with MS, leptin and VEGF levels are higher both in serum and in breath condensate than in subjects without MS. 116 Patients with obstructive sleep apnea (OSA) and MS; without OSA but with MS; and without OSA and without MS matched for gender, age, and central obesity have similar leptin and VEGF, serum levels.…”

Section: Human Studiesmentioning

confidence: 95%

Leptin–VEGF crosstalk in excess body mass and related disorders: A systematic review

Skrypnik

Suliburska

et al. 2023

Obesity Reviews

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Summary By 2030, it is expected that a billion people will have suffer from obesity. Adipose tissue synthesizes leptin, an adipokine that affects cardiovascular risk. Leptin intensifies the synthesis of vascular endothelial growth factor (VEGF). Our study reviews recent reports on leptin–VEGF crosstalk in obesity and related disorders. PubMed, Web of Science, Scopus, and Google Scholar were searched. One hundred and one articles involving human, animal, and in vitro research were included. In vitro studies show the crucial role of interaction between endothelial cells and adipocytes and hypoxia as a factor that intensifies leptin's effects on VEGF. Leptin–VEGF crosstalk promotes the progression of cancer. The animal research reveal that a high‐fat diet enhances leptin and VEGF crosstalk. Genetic and epigenetic mechanisms and procreator‐offspring programming may be involved in leptin–VEGF crosstalk. Some female‐specific characteristics of leptin–VEGF relation in obesity were observed. The human studies have shown that increased leptin and VEGF synthesis and leptin–VEGF crosstalk are factors linking obesity with elevated cardiovascular risk. The studies of the last 10 years documented a range of significant aspects of leptin–VEGF crosstalk specific for obesity and related disorders, shedding new light on the link between obesity and increased cardiovascular risk.

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Differential protein profiling as a potential multi-marker approach for obese patients with heart failure: A retrospective study

Cited by 5 publications

References 22 publications

Tumor-associated macrophages (TAMs) depend on MMP1 for their cancer-promoting role

Tumor-associated macrophages (TAMs) depend on MMP1 for their cancer-promoting role

Circulating proteomic signature of early death in heart failure patients with reduced ejection fraction

Leptin–VEGF crosstalk in excess body mass and related disorders: A systematic review

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