PPARγ Regulates Macrophage Polarization by Inhibiting the JAK/STAT Pathway and Attenuates Myocardial Ischemia/Reperfusion Injury In Vivo

Wang, Shengnan; Cai, Yu; Bu, Rongsheng; Wang, Yaoguo; Lin, Qingfan; Chen, Youfang; Wu, Chunchun

doi:10.1007/s12013-023-01137-0

Cited by 5 publications

(2 citation statements)

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“…In a mouse myocardial ischemia model, PPAR-γ was observed to regulate macrophage polarization through the inhibition of the JAK/STAT pathway. 19 Therefore, we believe that macrophages can inhibit inflammation and promote the survival of adipose grafts by promoting the polarization of M2 macrophages. However, blindly increasing M2 macrophages is not beneficial for the survival of adipose grafts and may even aggravate adipose tissue fibrosis 58 and inhibit the adipogenic process.…”

Section: Discussionmentioning

confidence: 99%

“…16 More importantly, PPAR-γ can inhibit the expression of proinflammatory cytokines during macrophage polarization through dependent or independent mechanisms to exert antiinflammatory effects. [17][18][19] Rosiglitazone, a PPAR-γ agonist, has been widely used in the clinic 20 and has anti-inflammatory, antifibrotic, and antioxidant properties. 21,22 In regulating adipose differentiation, rosiglitazone also plays an important role in inducing the browning of white adipose tissue (WAT), thereby promoting the survival and retention of fat grafts.…”

Section: Introductionmentioning

confidence: 99%

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PPAR‐γ regulates the polarization of M2 macrophages to improve the microenvironment for autologous fat grafting

Zhang,

Li,

Dong

et al. 2024

The FASEB Journal

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The unpredictable survival rate of autologous fat grafting (AFG) seriously affects its clinical application. Improving the survival rate of AFG has become an unresolved issue in plastic surgery. Peroxisome proliferator‐activated receptor‐γ (PPAR‐γ) regulates the adipogenic differentiation of adipocytes, but the functional mechanism in AFG remains unclear. In this study, we established an animal model of AFG and demonstrated the superior therapeutic effect of PPAR‐γ regulation in the process of AFG. From day 3 after fat grafting, the PPAR‐γ agonist rosiglitazone group consistently showed better adipose integrity, fewer oil cysts, and fibrosis. Massive macrophage infiltration was observed after 7 days. At the same time, M2 macrophages begin to appear. At day 14, M2 macrophages gradually became the dominant cell population, which suppressed inflammation and promoted revascularization and fat regeneration. In addition, transcriptome sequencing showed that the differentially expressed genes in the Rosiglitazone group were associated with the pathways of adipose regeneration, differentiation, and angiogenesis; these results provide new ideas for clinical treatment.

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Section: Discussionmentioning

confidence: 99%