Tacrolimus ameliorates bleomycin-induced pulmonary fibrosis by inhibiting M2 macrophage polarization via JAK2/STAT3 signaling

Liu, Bowen; Jiang, Qiuyan; Chen, Ruxuan; Gao, Shaoyan; Xia, Qing; Zhu, Jianming; Zhang, Fangxia; Shao, Chen; Liu, Xiangning; Li, Xiaohe; Zhou, Honggang; Yang, Cheng; Huang, Hui

doi:10.1016/j.intimp.2022.109424

Cited by 18 publications

(10 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, the M2 macrophage marker CD206 may be a potential target for PF treatment. Furthermore, JAK/STAT3 signaling plays a central role in M2 macrophage polarization, suggesting that the JAK/STAT3 signaling pathway participates in tissue fibrosis [ 68 , 69 ].…”

Section: Mechanisms Of Wound Healing and Fibrosismentioning

confidence: 99%

Immune Mechanisms of Pulmonary Fibrosis with Bleomycin

Ishida

Kuninaka

Mukaida

et al. 2023

IJMS

View full text Add to dashboard Cite

Fibrosis and structural remodeling of the lung tissue can significantly impair lung function, often with fatal consequences. The etiology of pulmonary fibrosis (PF) is diverse and includes different triggers such as allergens, chemicals, radiation, and environmental particles. However, the cause of idiopathic PF (IPF), one of the most common forms of PF, remains unknown. Experimental models have been developed to study the mechanisms of PF, and the murine bleomycin (BLM) model has received the most attention. Epithelial injury, inflammation, epithelial–mesenchymal transition (EMT), myofibroblast activation, and repeated tissue injury are important initiators of fibrosis. In this review, we examined the common mechanisms of lung wound-healing responses after BLM-induced lung injury as well as the pathogenesis of the most common PF. A three-stage model of wound repair involving injury, inflammation, and repair is outlined. Dysregulation of one or more of these three phases has been reported in many cases of PF. We reviewed the literature investigating PF pathogenesis, and the role of cytokines, chemokines, growth factors, and matrix feeding in an animal model of BLM-induced PF.

show abstract

Section: Mechanisms Of Wound Healing and Fibrosismentioning

confidence: 99%

Immune Mechanisms of Pulmonary Fibrosis with Bleomycin

Ishida

Kuninaka

Mukaida

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

“…Activation of these key transcription factors controls macrophage skewing toward the M1 phenotype or toward the M2 phenotype. Among them, STAT3, a member of the STATs family, has been shown to be involved in macrophage polarization and plays an important role in a variety of inflammatory-immune, fibrotic and neoplastic diseases (9)(10)(11). Therefore, this review used "STAT3", "macrophage polarization" and "signaling pathway" as search terms and searched PubMed, Web of Science and Google Scholar to summarize the relevant signaling pathways and their regulatory mechanisms of STAT3-regulated macrophage polarization, hoping to provide direction and basis for the mechanism research and therapeutic strategy development of related diseases involving STAT3 and macrophage polarization.…”

mentioning

confidence: 99%

Advances in the role of STAT3 in macrophage polarization

et al. 2023

View full text Add to dashboard Cite

The physiological processes of cell growth, proliferation, differentiation, and apoptosis are closely related to STAT3, and it has been demonstrated that aberrant STAT3 expression has an impact on the onset and progression of a number of inflammatory immunological disorders, fibrotic diseases, and malignancies. In order to produce the necessary biological effects, macrophages (M0) can be polarized into pro-inflammatory (M1) and anti-inflammatory (M2) types in response to various microenvironmental stimuli. STAT3 signaling is involved in macrophage polarization, and the research of the effect of STAT3 on macrophage polarization has gained attention in recent years. In order to provide references for the treatment and investigation of disorders related to macrophage polarization, this review compiles the pertinent signaling pathways associated with STAT3 and macrophage polarization from many fundamental studies.

show abstract

“…Macrophages have been reported to be involved in inflammatory response during IDD progression ( 30 , 31 ). As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

CX3CL1/CX3CR1 axis alleviates inflammation and apoptosis in human nucleus pulpous cells via M2 macrophage polarization

Gao

Xie

et al. 2023

Exp Ther Med

View full text Add to dashboard Cite

CX3C chemokine ligand 1 (CX3CL1) belongs to the CX3C chemokine family and is involved in various disease processes. However, its role in intervertebral disc degeneration (IDD) remains to be elucidated. In the present study, western blotting, reverse transcription-quantitative PCR and ELISA assays were used to assess target gene expression. In addition, immunofluorescence and TUNEL staining were used to assess macrophage infiltration, monocyte migration and apoptosis. The present study aimed to reveal if and how CX3CL1 regulates IDD progression by exploring its effect on macrophage polarization and apoptosis of human nucleus pulposus cells (HNPCs). The data showed that CX3CL1 bound to CX3C motif chemokine receptor 1 (CX3CR1) promoted the M2 phenotype polarization via JAK2/STAT3 signaling, followed by increasing the secretion of anti-inflammatory cytokines from HNPCs. In addition, HNPC-derived CX3CL1 promoted M2 macrophage-derived C-C motif chemokine ligand 17 release thereby reducing the apoptosis of HNPCs. In clinic, the reduction of mRNA and protein levels CX3CL1 in degenerative nucleus pulposus tissues (NPs) was measured. Increased M1 macrophages and pro-inflammatory cytokines were found in NPs of IDD patients with low CX3CL1 expression. Collectively, these findings suggested that the CX3CL1/CX3CR1 axis alleviates IDD by reducing inflammation and apoptosis of HNPCs via macrophages. Therefore, targeting CX3CL1/CX3CR1 axis is expected to produce a new therapeutic approach for IDD.

show abstract

Tacrolimus ameliorates bleomycin-induced pulmonary fibrosis by inhibiting M2 macrophage polarization via JAK2/STAT3 signaling

Cited by 18 publications

References 25 publications

Immune Mechanisms of Pulmonary Fibrosis with Bleomycin

Immune Mechanisms of Pulmonary Fibrosis with Bleomycin

Advances in the role of STAT3 in macrophage polarization

CX3CL1/CX3CR1 axis alleviates inflammation and apoptosis in human nucleus pulpous cells via M2 macrophage polarization

Contact Info

Product

Resources

About