ArticleMolecular medicine reports2020
Angiotensin II induces RAW264.7 macrophage polarization to the M1‑type through the connexin 43/NF‑κB pathway.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 25 citations in OpenAlex.
- Early atherogenesis: In search of etiology.International journal of cardiology. Cardiovascular risk and prevention · 2026Review
- Conditional ablation of RGS2 in myeloid cells does not influence blood pressure and organ damage in angiotensin II-induced hypertension in mice.Physiological reports · 2026Article
- Magnetic Reprogramming of Macrophages Stimulates Phagocytosis of Breast Cancer Cells via a TRPC1-STING Inflammatory Axis.Smart medicine · 2026Article
- Nano-in-Micro GelMA depots assist electro-thermal-immuno orchestral treatment for solid triple negative breast tumor.Materials today. Bio · 2026Article
- A Dual-Network Injectable Hydrogel Scaffold Integrating Glycyrrhizic Acid and Acellular Fat Extracts for Synergistic Enhancement of Diabetic Wound Healing.ACS polymers Au · 2026Article
- Macrophagic Sclerostin Loop2-ApoER2 Interaction Required by Sclerostin for Cardiovascular Protective Action.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting the PI3K/Akt/NF-κB axis: Cluster of differentiation 5-like-mediated immunometabolic regulation of macrophage polarization in abdominal aortic aneurysm.Journal of cell communication and signaling · 2025Article
- Anti PD-L1 immunotherapy alters macrophage phenotypes via EGR1 and HSP90AB1 supported by integrated methodologies.Scientific reports · 2025Article
- Immunology of Hypertension: Pathophysiological and Therapeutic Aspects.International journal of molecular sciences · 2025Review
- An active shrinkage and antioxidative hydrogel with biomimetic mechanics functions modulates inflammation and fibrosis to promote skin regeneration.Bioactive materials · 2025Article
- Coordination of innate immune responses by connexins.Frontiers in immunology · 2025Review
- Parishin E from ginger-processedFrontiers in pharmacology · 2025Article
- Modulator Effect of AT1 Receptor Knockdown on THP-1 Macrophage Proinflammatory Activity.Biology · 2024Article
- Article
- Targeting Macrophages: Therapeutic Approaches in Diabetic Kidney Disease.International journal of molecular sciences · 2024Review
- The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023Review
- Article
- Losartan modifies mesh integration after abdominal wall repair: an experimental study.Hernia : the journal of hernias and abdominal wall surgery · 2022Article
- Bone Marrow Origin of Coronary Artery Diseases: The Impact of the Local Renin-Angiotensin System.Acta Cardiologica Sinica · 2022Review
- Regulation of Monocytes/Macrophages by the Renin-Angiotensin System in Diabetic Nephropathy: State of the Art and Results of a Pilot Study.International journal of molecular sciences · 2021Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiotensin II (AngII) serves an important inflammatory role in cardiovascular disease; it can induce macrophages to differentiate into the M1‑type, produce inflammatory cytokines and resist pathogen invasion, and can cause a certain degree of damage to the body. Previous studies have reported that connexin 43 (Cx43) and NF‑κB (p65) are involved in the AngII‑induced inflammatory pathways of macrophages; however, the mechanisms underlying the effects of Cx43 and NF‑κB (p65) on AngII‑induced macrophage polarization have not been determined. Thus, the present study aimed to investigate the effects of Cx43 and NF‑κB (p65) on the polarization process of AngII‑induced macrophages. The macrophage polarization‑related proteins and mRNAs were examined by flow cytometry, western blotting, immunofluorescence, ELISA and reverse transcription‑quantitative PCR analyses. RAW264.7 macrophages were treated with AngII to simulate chronic inflammation and it was subsequently found that AngII promoted RAW 264.7 macrophage polarization towards the M1‑type by such effects as the release of inducible nitric oxide synthase (iNOS), tumour necrosis factor (TNF)‑α, IL‑1β, the secretion of IL‑6, and the expression of M1‑type indicators, such as CD86. Simultaneously, compared with the control group, the protein expression levels of Cx43 and phosphorylated (p)‑p65 were significantly increased following AngII treatment. The M1‑related phenotypic indicators, iNOS, TNF‑α, IL‑1β, IL‑6 and CD86, were inhibited by the NF‑κB (p65) signalling pathway inhibitor BAY117082. Similarly, the Cx43 inhibitors, Gap26 and Gap19, also inhibited the expression of M1‑related factors, and the protein expression levels of p‑p65 in the Gap26/Gap19 groups were significantly decreased compared with the AngII group. Altogether, these findings suggested that AngII may induce the polarization of RAW264.7 macrophages to the M1‑type through the Cx43/NF‑κB (p65) signalling pathway.
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