Verdiperstat attenuates acute lung injury by modulating MPO/μ-calpain/β-catenin signaling

Ren, Rui; Xu, Zehui; Wang, Xin; Jiang, Wanglin; Yu, Pengfei

doi:10.1016/j.ejphar.2022.174940

Cited by 7 publications

(3 citation statements)

References 18 publications

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“…In LPS-treated mice, the lung wet/dry ratio and protein concentration in BALF were significantly increased ( Figure 5 A-B). Myeloperoxidase (MPO), a neutrophil marker, indicates the degree of inflammatory cell infiltration and the progression of lung injury in ALI [ 28 ]. In the lung tissues of LPS-treated mice, the total cell count, percentage of neutrophils, and MPO activity were all higher than in wild-type mice (Figures.…”

Section: Resultsmentioning

confidence: 99%

TM9SF1 knockdown decreases inflammation by enhancing autophagy in a mouse model of acute lung injury

Xiao¹,

Shen²,

Chen³

et al. 2022

Heliyon

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Section: Resultsmentioning

confidence: 99%

TM9SF1 knockdown decreases inflammation by enhancing autophagy in a mouse model of acute lung injury

Xiao¹,

Shen²,

Chen³

et al. 2022

Heliyon

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“…Although no significant protective effects have been seen in phase III trials for the treatment of multiple-system atrophy, it has demonstrated efficacy in amyotrophic lateral sclerosis (NCT04436510). Several researchers have studied AZD3241 at the animal level for other disease applications, such as ALI [232], and some results have been achieved both in vitro (a reduced distribution of β-catenin in the nuclei of pulmonary microvascular endothelial cells after treatment with AZD3241) and in vivo (decreased lung coefficient and pathology scores in a rat ALI model injected with AZD3241). Also, this inhibitor could help improve the response in immune checkpoint therapy for patients with melanoma and immune checkpoint therapy resistance for melanoma [233].…”

Section: Mpo Inhibitors In Clinical Trialsmentioning

confidence: 99%

The Roles of Neutrophil-Derived Myeloperoxidase (MPO) in Diseases: The New Progress

Lin,

Chen,

Chen

et al. 2024

Antioxidants

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Myeloperoxidase (MPO) is a heme-containing peroxidase, mainly expressed in neutrophils and, to a lesser extent, in monocytes. MPO is known to have a broad bactericidal ability via catalyzing the reaction of Cl− with H2O2 to produce a strong oxidant, hypochlorous acid (HOCl). However, the overproduction of MPO-derived oxidants has drawn attention to its detrimental role, especially in diseases characterized by acute or chronic inflammation. Broadly speaking, MPO and its derived oxidants are involved in the pathological processes of diseases mainly through the oxidation of biomolecules, which promotes inflammation and oxidative stress. Meanwhile, some researchers found that MPO deficiency or using MPO inhibitors could attenuate inflammation and tissue injuries. Taken together, MPO might be a promising target for both prognostic and therapeutic interventions. Therefore, understanding the role of MPO in the progress of various diseases is of great value. This review provides a comprehensive analysis of the diverse roles of MPO in the progression of several diseases, including cardiovascular diseases (CVDs), neurodegenerative diseases, cancers, renal diseases, and lung diseases (including COVID-19). This information serves as a valuable reference for subsequent mechanistic research and drug development.

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“…Research has shown that Ruscogenin upregulates the expression of p120 catenin and VE-cadherin via inactivating the TLR4/Src signaling in mice with sepsis-induced ALI [ 170 ]. Verdiperstat, a myeloperoxidase inhibitor, enhances VE-cadherin stability by reducing the activation of myeloperoxidase/μ-calpain/β-catenin signaling pathway on experimental ARDS in rats [ 269 ]. Blebbistatin is a myosin II inhibitor that resists pulmonary endothelial barrier dysfunction in mice.…”

Section: Emerging Pharmacologic Therapies For Ardsmentioning

confidence: 99%

Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS)

Huang,

Le,

et al. 2024

Respir Res

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Acute respiratory distress syndrome (ARDS) is a common condition associated with critically ill patients, characterized by bilateral chest radiographical opacities with refractory hypoxemia due to noncardiogenic pulmonary edema. Despite significant advances, the mortality of ARDS remains unacceptably high, and there are still no effective targeted pharmacotherapeutic agents. With the outbreak of coronavirus disease 19 worldwide, the mortality of ARDS has increased correspondingly. Comprehending the pathophysiology and the underlying molecular mechanisms of ARDS may thus be essential to developing effective therapeutic strategies and reducing mortality. To facilitate further understanding of its pathogenesis and exploring novel therapeutics, this review provides comprehensive information of ARDS from pathophysiology to molecular mechanisms and presents targeted therapeutics. We first describe the pathogenesis and pathophysiology of ARDS that involve dysregulated inflammation, alveolar-capillary barrier dysfunction, impaired alveolar fluid clearance and oxidative stress. Next, we summarize the molecular mechanisms and signaling pathways related to the above four aspects of ARDS pathophysiology, along with the latest research progress. Finally, we discuss the emerging therapeutic strategies that show exciting promise in ARDS, including several pharmacologic therapies, microRNA-based therapies and mesenchymal stromal cell therapies, highlighting the pathophysiological basis and the influences on signal transduction pathways for their use.

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Verdiperstat attenuates acute lung injury by modulating MPO/μ-calpain/β-catenin signaling

Cited by 7 publications

References 18 publications

TM9SF1 knockdown decreases inflammation by enhancing autophagy in a mouse model of acute lung injury

TM9SF1 knockdown decreases inflammation by enhancing autophagy in a mouse model of acute lung injury

The Roles of Neutrophil-Derived Myeloperoxidase (MPO) in Diseases: The New Progress

Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS)

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