The Apelin-APJ axis alleviates LPS-induced pulmonary fibrosis and endothelial mesenchymal transformation in mice by promoting Angiotensin-Converting Enzyme 2

Wang, Hui; Cong, Linjing; Yin, Xianghong; Zhang, Nan; Zhu, Meifang; Sun, Tao; Fan, Junming; Xue, Feng; Fan, Xiaofang; Gong, Yanling

doi:10.1016/j.cellsig.2022.110418

Cited by 10 publications

(8 citation statements)

References 40 publications

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“…In a mouse model of LPSinduced pulmonary fibrosis, Apelin-APJ was found to inhibit the ubiquitination of ACE2, thereby upregulating its expression and alleviating mesenchymal transition of endothelial cells and pulmonary fibrosis. 91 These findings collectively reveal the regulatory role of ACE2 ubiquitination in RAS-related diseases and provide a theoretical basis for the treatment of lung fibrosis and cardiovascular diseases.…”

Section: Ubiquitination Of Ace2mentioning

confidence: 72%

Posttranslational modifications of ACE2 protein: Implications for SARS‐CoV‐2 infection and beyond

Xiao,

Chang,

et al. 2023

Journal of Medical Virology

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The present worldwide pandemic of coronavirus disease 2019 (COVID‐19) has highlighted the important function of angiotensin‐converting enzyme 2 (ACE2) as a receptor for severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) entry. A deeper understanding of ACE2 could offer insights into the mechanisms of SARS‐CoV‐2 infection. While ACE2 is subject to regulation by various factors in vivo, current research in this area is insufficient to fully elucidate the corresponding pathways of control. Posttranslational modification (PTM) is a powerful tool for broadening the variety of proteins. The PTM study of ACE2 will help us to make up for the deficiency in the regulation of protein synthesis and translation. However, research on PTM‐related aspects of ACE2 remains limited, mostly focused on glycosylation. Accordingly, a comprehensive review of ACE2 PTMs could help us better understand the infection process and provide a basis for the treatment of COVID‐19 and beyond.

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Section: Ubiquitination Of Ace2mentioning

confidence: 72%

Posttranslational modifications of ACE2 protein: Implications for SARS‐CoV‐2 infection and beyond

Xiao,

Chang,

et al. 2023

Journal of Medical Virology

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“…Referring to pulmonary fibrosis, several studies affirmed that apelin participated in the process of melatonin alleviating bleomycin-induced pulmonary injury and evodiamine alleviating lipopolysaccharide-induced pulmonary inflammation and fibrosis 47 , 49 . Apelin can also directly alleviate lipopolysaccharide-induced pulmonary fibrosis in mice by promoting angiotensin-converting enzyme 2 50 or suppressing TGF-β1 signaling 51 . However, to date, most research focused on the protective effect of apelin on fibrosis by administrating apelin before or immediately after the stimulation 50 , 51 .…”

Section: Discussionmentioning

confidence: 99%

Apelin Prevents and Alleviates Crystalline Silica-induced Pulmonary Fibrosis via Inhibiting Transforming Growth Factor Beta 1-triggered Fibroblast Activation

Shen¹,

Feng²,

Wu³

et al. 2023

Int. J. Biol. Sci.

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Silicosis is a common and ultimately fatal occupational disease, yet the limited therapeutic option remains the major clinical challenge. Apelin, an endogenous ligand of the G-protein-coupled receptor (APJ), is abundantly expressed in diverse organs. The apelin-APJ axis helps to control pathological and physiological processes in lung. The role of apelin in the pathological process and its possible therapeutic effects on silicosis have not been elucidated. In this study, we found that lung expression and circulating levels of apelin were markedly decreased in silicosis patients and silica-induced fibrotic mice and associated with the severity. Furthermore, in vivo data demonstrated that pre-treatment from day 3 and post-treatment from day 15 with apelin could both alleviate silica-induced pulmonary fibrosis in mice. Besides, apelin inhibited pulmonary fibroblast activation via transforming growth factor beta 1 (TGF-β1) signaling. Our study suggested that apelin could prevent and reverse silica-induced pulmonary fibrosis by inhibiting the fibroblast activation through TGF-β1 signaling pathway, thus providing a new potential therapeutic strategy for silicosis and other pulmonary fibrosis.

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“… 92 LPS-induced ALI/ARDS and pulmonary fibrosis mimic sepsis-related pulmonary ALI and pulmonary fibrosis. 93 …”

Section: The Involvement Of the Apelin/apj System In Septic Conditionsmentioning

confidence: 99%

“… 101 Apelin was shown to promote ACE2 expression, thereby reducing endothelial-mesenchymal transition and preventing sepsis-associated pulmonary fibrosis in mice. 93 Additionally, inhibition of APJ exacerbated pulmonary fibrosis. This is further evidence of the protective role of the Apelin/APJ system against organ damage in sepsis.…”

Section: The Involvement Of the Apelin/apj System In Septic Conditionsmentioning

confidence: 99%

The Apelin/APJ System: A Potential Therapeutic Target for Sepsis

Song,

Wang,

Cao

et al. 2024

JIR

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Apelin is the native ligand for the G protein-coupled receptor APJ. Numerous studies have demonstrated that the Apelin/APJ system has positive inotropic, anti-inflammatory, and anti-apoptotic effects and regulates fluid homeostasis. The Apelin/APJ system has been demonstrated to play a protective role in sepsis and may serve as a promising therapeutic target for the treatment of sepsis. Better understanding of the mechanisms of the effects of the Apelin/APJ system will aid in the development of novel drugs for the treatment of sepsis. In this review, we provide a brief overview of the physiological role of the Apelin/APJ system and its role in sepsis.

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The Apelin-APJ axis alleviates LPS-induced pulmonary fibrosis and endothelial mesenchymal transformation in mice by promoting Angiotensin-Converting Enzyme 2

Cited by 10 publications

References 40 publications

Posttranslational modifications of ACE2 protein: Implications for SARS‐CoV‐2 infection and beyond

Posttranslational modifications of ACE2 protein: Implications for SARS‐CoV‐2 infection and beyond

Apelin Prevents and Alleviates Crystalline Silica-induced Pulmonary Fibrosis via Inhibiting Transforming Growth Factor Beta 1-triggered Fibroblast Activation

The Apelin/APJ System: A Potential Therapeutic Target for Sepsis

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