Macrophage migration inhibitory factor (MIF) in the development and progression of pulmonary arterial hypertension

Ahmed, Mohamed; Miller, Edmund J.

doi:10.21542/gcsp.2018.14

Cited by 8 publications

(6 citation statements)

References 137 publications

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“…Hypoxia, as the main driver of PH, lead to increased levels of macrophage migration inhibitory factor (MIF) in the monocyte-macrophage system, thereby activating NF-κB and p38 mitogen-activated protein kinase (p38MAPK) pathways to regulate IL-6 ( 37 , 89 , 90 ). Thyroxine T4 is a natural ligand inhibitor of MIF, which can inhibit the inflammatory activity of MIF by blocking the MIF site, and different anti-MIF treatments achieve good efficacy in animal models ( Table 1 ) ( 37 ).…”

Section: Pathogenesis and Pathways Of Il-6 In Phmentioning

confidence: 99%

Interleukin-6 and pulmonary hypertension: from physiopathology to therapy

et al. 2023

Front. Immunol.

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Pulmonary hypertension (PH) is a progressive, pulmonary vascular disease with high morbidity and mortality. Unfortunately, the pathogenesis of PH is complex and remains unclear. Existing studies have suggested that inflammatory factors are key factors in PH. Interleukin-6 (IL-6) is a multifunctional cytokine that plays a crucial role in the regulation of the immune system. Current studies reveal that IL-6 is elevated in the serum of patients with PH and it is negatively correlated with lung function in those patients. Since IL-6 is one of the most important mediators in the pathogenesis of inflammation in PH, signaling mechanisms targeting IL-6 may become therapeutic targets for this disease. In this review, we detailed the potential role of IL-6 in accelerating PH process and the specific mechanisms and signaling pathways. We also summarized the current drugs targeting these inflammatory pathways to treat PH. We hope that this study will provide a more theoretical basis for targeted treatment in patients with PH in the future.

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Section: Pathogenesis and Pathways Of Il-6 In Phmentioning

confidence: 99%

Interleukin-6 and pulmonary hypertension: from physiopathology to therapy

et al. 2023

Front. Immunol.

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“…IL-6 is a pro-inflammatory cytokine highly associated with PH pathogenesis. Additionally, IL-6 is also activated by an upstream inflammatory cytokine known as the macrophage migration inhibitory factor, which further propagates the development of a chronic inflammatory immune response ( 100 ). Patients with PH have elevated plasma IL-6 ( 98 , 101 ) and MCP-1 ( 102 ) levels, and in cases of severe disease, reduced PPAR-γ ( 103 ).…”

Section: Antenatal Cdh-ph Pharmacotherapiesmentioning

confidence: 99%

Emerging antenatal therapies for congenital diaphragmatic hernia-induced pulmonary hypertension in preclinical models

et al. 2020

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Congenital diaphragmatic hernia (CDH)-related deaths are the largest contributor of in-hospital neonatal deaths in children with congenital malformations. Morbidity and mortality in CDH are directly related to the development of pulmonary hypertension (PH). Current treatment consists of supportive measures. To date, no pharmacotherapy has been shown to effectively reverse the hallmark finding of pulmonary vascular remodeling that is associated with pulmonary hypertension in CDH (CDH-PH). As such, there is a great need for novel therapies to effectively manage CDH-PH. Our review aims to evaluate emerging therapies, and specifically focuses on those that are still under investigation and not approved for clinical use by the Food and Drug Administration. Therapies were categorized into antenatal pharmacotherapies or antenatal regenerative therapies and assessed on their method of administration, safety profile, effect on pulmonary vascular pathophysiology, and overall efficacy. In general, emerging antenatal pharmaceutical and regenerative treatments primarily aim to alleviate pulmonary vascular remodeling by restoring normal function and levels of key regulatory factors involved in pulmonary vascular development and/or in promoting angiogenesis. Overall, while these emerging therapies show great promise for the management of CDH-PH, most require further assessment of safety and efficacy in preclinical models before translation into the clinical setting.

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“…Persistent right-left leakage at the level of the patent ductus arteriosus (PDA) and subsequent disturbances in blood distribution within organs, may result in an increased incidence of intraventricular haemorrhage (IVH), necrotizing enterocolitis (NEC), and retinopathy of prematurity (ROP) and also BPD [30][31][32][33][34][35]. Increased blood flow through the pulmonary vessels results in damage to the capillaries of the interstitial septa, and consequently, the migration of neutrophils to interstitial tissue [11,35,36]. In the case of MV using high inspiratory pressures, pulmonary distension and activation of macrophages within the alveoli and extravasated neutrophils from damaged capillaries may occur, resulting in increased production of pro-inflammatory cytokines, mainly IL-12 and TNF-α [11,37,38].…”

Section: Risk Factors and Pathophysiological Mechanisms Of Bpdmentioning

confidence: 99%

Pathophysiological mechanisms and pharmacological methods of prevention and treatment of bronchopulmonary dysplasia in preterm infants

Wątroba¹,

Bryda²

2019

J Pre Clin Clin Res.

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Wątroba S. J, Bryda J. Pathophysiological mechanisms and pharmacological methods of prevention and treatment of bronchopulmonary dysplasia in preterm infants. AbstractIntroduction. Bronchopulmonary dysplasia (BPD) is a respiratory disease that is characterized by long-term respiratory failure and mainly affects premature infants with low birth weight (LBW), undergoing mechanical ventilation (MV) or requiring long-term oxygen therapy. In Europe, among newborns with birth weight <1500g, the incidence of BPD is around 15%. Objective. The purpose of this review was to analyze the pathophysiological mechanisms involved in the development of BPD in premature newborns and to discuss the current possibilities of pharmacological prevention and treatment of BPD. Description of the state of knowledge. The BPD pathogenesis is multifactorial. Lung damage is the result of barotrauma and volutrauma due to high-performance MV, actions of reactive oxygen species (ROS) and infectious agents. Currently used methods of pharmacological treatment of severe forms of BPD are mainly based on systemic steroid therapy and can not be considered completely effective and free of side effects. Conclusion. Despite the widespread use of proper pharmacotherapy and dynamic development of new methods of respiratory therapy, mortality in BPD is estimated at around 10% -20%. Infants with BPD are much more exposed to respiratory infections caused by respiratory syncytial virus (RSV), which may result in the development of bronchial hyperresponsiveness and bronchial asthma. Among children with BPD there are significantly higher cognitive and behavioral deficits compared to healthy children, and cerebral palsy is also significantly more common.Abbreviations AA -arachidonic acid; AAP COFN -Committee on Foetus and Newborn of the American Academy of Pediatrics; ACTHadrenocorticotropin; ADH -vasopressin, antidiuretic hormone; ASMC -airway smooth muscle cells; BPD -bronchopulmonary dysplasia; BTN -betamethasone; CAT -catalase; CC10 -Clara cell 10 kDa protein; CLD -chronic lung disease; COXcyclooxygenase; CPAP -continuous positive airway pressure; CPS FNC -Fetus and Newborn Committee of the Canadian Pediatric Society; DEX -dexamethasone; ELBW -extremely low birth weight; ENA-78 -epithelial protein activating neutrophils; EURAIL -Europe Against Immature Lung; FC -fludrocortisone; FiO 2 -oxygen concentration in the breathing mixture; FTP -fluticasone propionate; GCSs -glucocorticosteroids; GM-CSF -granulocyte and macrophage colonystimulating factor; GPx -glutathione peroxidase; HC -hydrocortisone; HO . -hydroxyl radical; HO 2 . -hydroperoxide radical; IFN-γ -gamma interferon; ILs -interleukins; IRDS -respiratory distress syndrome; IUGR -intrauterine growth retardation; IVH -intraventricular haemorrhage; LBW -low birth weight; LTs -leukotrienes; MAS -meconium aspiration syndrome; MIP-1 -macrophage inflammatory protein-1; MMPs -metalloproteinases; MRI -magnetic resonance imaging; MV -mechanical ventilation; n-CPAP -continuous positive airway pressure -nasal metho...

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Macrophage migration inhibitory factor (MIF) in the development and progression of pulmonary arterial hypertension

Cited by 8 publications

References 137 publications

Interleukin-6 and pulmonary hypertension: from physiopathology to therapy

Interleukin-6 and pulmonary hypertension: from physiopathology to therapy

Emerging antenatal therapies for congenital diaphragmatic hernia-induced pulmonary hypertension in preclinical models

Pathophysiological mechanisms and pharmacological methods of prevention and treatment of bronchopulmonary dysplasia in preterm infants

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