Circulating macrophage migration inhibitory factor (MIF) in patients with heart failure

Luedike, Peter; Alatzides, Georgios; Παπαθανασίου, Μαρία; Heisler, Martin; Pohl, Julia; Lehmann, Nils; Rassaf, Tienush

doi:10.1016/j.cyto.2018.04.033

Cited by 18 publications

(13 citation statements)

References 22 publications

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“…9). Although a plethora of studies has demonstrated the pathogenic roles of MIF, a variety of medical complications, such as heart failure, type two diabetes, and rheumatoid arthritis in the past decades (48)(49)(50)(51), and MIF's role in the bone pathophysiology remains controversial. Our group and others reported that MIF promotes osteoclastogenesis in vitro and upregulates the pathogenic bone resorption in various mouse models of osteolytic lesions (16,19,21).…”

Section: Discussionmentioning

confidence: 99%

Elevated Expression of Macrophage Migration Inhibitory Factor Promotes Inflammatory Bone Resorption Induced in a Mouse Model of Periradicular Periodontitis

Howait

Albassam

Yamada

et al. 2019

The Journal of Immunology

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Locally produced osteoclastogenic factor RANKL plays a critical role in the development of bone resorption in periradicular periodontitis. However, because RANKL is also required for healthy bone remodeling, it is plausible that a costimulatory molecule that upregulates RANKL production in inflammatory periradicular periodontitis may be involved in the pathogenic bone loss processes. We hypothesized that macrophage migration inhibitory factor (MIF) would play a role in upregulating the RANKL-mediated osteoclastogenesis in the periradicular lesion. In response to pulp exposure, the bone loss and level of MIF mRNA increased in the periradicular periodontitis, which peaked at 14 d, in conjunction with the upregulated expressions of mRNAs for RANKL, proinflammatory cytokines (TNF-a, IL-6, and IL-1b), chemokines (MCP-1 and SDF-1), and MIF's cognate receptors CXCR4 and CD74. Furthermore, expressions of those mRNAs were found significantly higher in wild-type mice compared with that of MIF 2/2 mice. In contrast, bacterial LPS elicited the production of MIF from ligament fibroblasts in vitro, which, in turn, enhanced their productions of RANKL and TNF-a. rMIF significantly upregulated the number of TRAP + osteoclasts in vitro. Finally, periapical bone loss induced in wild-type mice were significantly diminished in MIF 2/2 mice. Altogether, the current study demonstrated that MIF appeared to function as a key costimulatory molecule to upregulate RANKL-mediated osteoclastogenesis, leading to the pathogenically augmented bone resorption in periradicular lesions. These data also suggest that the approach to neutralize MIF activity may lead to the development of a therapeutic regimen for the prevention of pathogenic bone loss in periradicular periodontitis.

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Section: Discussionmentioning

confidence: 99%

Elevated Expression of Macrophage Migration Inhibitory Factor Promotes Inflammatory Bone Resorption Induced in a Mouse Model of Periradicular Periodontitis

Howait

Albassam

Yamada

et al. 2019

The Journal of Immunology

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“…In addition, MIF levels were also found to correlate with markers of heart failure, the level of natriuretic peptides BNP and NT-proBNP, and a combined endpoint of death or hospitalization after 180 days. These results suggest that MIF could be a useful biomarker, as it is associated with clinical outcomes and could be involved in the pathophysiology of patients with HFpEF and PH (41,42).…”

Section: Elevated Levels Of Mif In Other Types Of Ph A) Ph Associatedmentioning

confidence: 82%

Multiple roles of macrophage migration inhibitory factor in pulmonary hypertension

Jalce¹,

Guignabert

2020

American Journal of Physiology-Lung Cellular and Molecular Phys

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Pulmonary hypertension (PH) is a life-threatening condition arising from the loss and obstructive remodeling of the pulmonary arteries, leading to the sustained elevation of pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR) and subsequently right ventricular (RV) failure and death. PH encompasses a group of multifactorial diseases, such as pulmonary arterial hypertension (PAH) and chronic thromboembolic PH, for which there is no treatment that can stop or reverse the progression of remodeling of the pulmonary vasculature. The identification of new molecular targets for the development of more effective drugs is thus urgently needed. In this context, macrophage migration inhibitory factor (MIF), a pleiotropic upstream proinflammatory mediator, is emerging as a promising molecular target, as it contributes to perivascular inflammation and pulmonary arterial remodeling, two key hallmarks of PAH that are not specifically targeted by currently approved therapies. The objective of this review is to summarize the scientific evidence on the pathogenic roles of MIF and its potential as a biomarker and therapeutic target in PH/PAH.

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“…Although previously it has been determined the fact of strong positive association between elevated levels of MIF and poor clinical outcomes in STEMI patients [28,29] , we first reported that similar relation could be determined in STEMI patients underwent successful reperfusion procedure. In this context, we can agree that MIF might become a target molecule for cardioprotective response in the future, while there are controversial issue regarding this assumption [30] .…”

Section: Discussionmentioning

confidence: 96%

“…However, negative impact on survival of both HF phenotypes is similar. Indeed, Luedike P et al [30,31] 2018 have shown a strong positive association between serum levels of MIF with 180-day HF clinical outcomes, all-cause death and hospitalization in patients with HFpEF. Interestingly, MIF has been also found as independent from conventional cardiovascular risk factors the predictor of impaired cardiac function and long-term prognosis in patients with AMI and HF [32,33] .…”

Section: Discussionmentioning

confidence: 99%

Prognostication of Late Cardiac Remodeling in Patients With STEMI Underwent Successful Percutaneous Coronary Intervention: the Role of Macrophage Inhibitory Factor

Petyunina

Kopytsya

Berezin³

2019

Journal of Cardiology and Therapy

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BACKGROUND: Macrophage inhibitory factor (MIF) plays a pivotal role in late adverse cardiac remodeling in acute ST-segment elevation myocardial infarction (STEMI). The aim of the study was to investigate the predictive role of the circulating MIF in adverse cardiac remodeling in STEMI patients undergoing percutaneous coronary intervention (PCI). METHODS: A total of 73 patients with confirmed acute STEMI successfully treated with PCI were enrolled for participation in the study. Control group was included 20 healthy volunteers. All patients signed informed consent to participate in the study. Echo and Doppler, biomarker assay and MIF determinations were performed at baseline and at 6 month after study entry. RESULTS: There were significant differences (p < 0.001) between the levels of MIF in control group (573.75 ng/mL; 95% CI = 397.80 to 1016.75 ng/mL) and entire STEMI patient population (2582.80 ng/mL; 95% CI = 1308.40 to 4122.20 ng/mL). The entire STEMI patient population was divided by the median of the MIF level as follow: the first group consisted of STEMI patients with MIF ≤ 2582.80 ng/ mL (n = 36), and the second group consisted of STEMI patients with the levels of MIF > 2582.80 ng/mL (n = 37). We found that cutoff MIF level ≥ 2644.5 ng/ml at baseline predicted adverse cardiac remodeling (AUC = 0.736, 95% CІ = 0.515 to 0.956, p = 0.0362; sensitivity = 72.7%; specificity = 81.8%; positive predictive value = 52.7%; negative predictive value = 32.4%; positive likelihood ratio = 0.89 and negative likelihood ratio = 0.72). CONCLUSIONS: The MIF level ≥ 2644.5 ng/mL might be predictor for late adverse cardiac remodeling after STEMI.

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Circulating macrophage migration inhibitory factor (MIF) in patients with heart failure

Cited by 18 publications

References 22 publications

Elevated Expression of Macrophage Migration Inhibitory Factor Promotes Inflammatory Bone Resorption Induced in a Mouse Model of Periradicular Periodontitis

Elevated Expression of Macrophage Migration Inhibitory Factor Promotes Inflammatory Bone Resorption Induced in a Mouse Model of Periradicular Periodontitis

Multiple roles of macrophage migration inhibitory factor in pulmonary hypertension

Prognostication of Late Cardiac Remodeling in Patients With STEMI Underwent Successful Percutaneous Coronary Intervention: the Role of Macrophage Inhibitory Factor

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