ArticleBioscience reports2020
ALK5 deficiency inhibits macrophage inflammation and lipid loading by targeting KLF4.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Unraveling fibrinogen-like protein 1's role in immune regulation.Frontiers in immunology · 2026Review
- A regulatory loop involving the cytochrome P450-soluble epoxide hydrolase axis and TGF-β signaling.iScience · 2024Article
- The Kruppel-like factor 4-signal transducer and activator of transcription 5A axis promotes pancreatic fibrosis in mice with caerulein-induced chronic pancreatitis.Experimental animals · 2023Article
- [Effects of Krüppel-like factor 4 on inflammatory response and organ injury in septic mice].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2022Article
- Macrophage TGF-β signaling is critical for wound healing with heterotopic ossification after trauma.JCI insight · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transforming growth factor type-β (TGF-β) has been demonstrated to play an important role in the development of atherosclerosis through binding to the serine/threonine kinase transmembrane type I and type II receptors. However, as a key type I receptor for TGF-β, the exact role and the underlying mechanism of Activin receptor-like kinase 5 (ALK5) on macrophage activation involved in atherogenesis remain unclear. In the present study, enhanced ALK5 expression was found in bone marrow derived macrophages (BMDMs) upon OX-LDL stimulation tested by RT-PCR and Western blot, which was further verified by co-immunofluorescence staining. Next, the loss-of-function of ALK5 used AdshALK5 transfection was performed to test the effect of ALK5 on macrophage activation. We observed that ALK5 silencing inhibited pro-inflammatory but promoted anti-inflammatory macrophage markers expression. Moreover, decreased foam cell formation was found in ALK5 knockdown macrophages accompanied by increased cholesterol efflux. Mechanistically, ALK5 knockdown significantly increased KLF4 expression that was responsible for the attenuated macrophage activation induced by ALK5 knockdown. Collectively, these findings suggested that neutralization of ALK5 may act as a promising strategy for the management of atherosclerosis.
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