Hypoxia inducible factor-1α is an important regulator of macrophage biology

Qiu, Bingquan; Yuan, Piaoliu; Du, Xiaojuan; Jin, Hongfang; Du, Junbao; Huang, Yaqian

doi:10.1016/j.heliyon.2023.e17167

Cited by 12 publications

(6 citation statements)

References 73 publications

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“…The LPS and hypoxic environment could induce RAW264.7 cells to upregulate the expression of HIF-1α, which could be effectively inhibited by the treatment, especially under the augmentation of US (Figure I,J). Therefore, we confirmed by in vitro experiments that the CuAP could effectively scavenge ROS, ameliorate hypoxia in cells, and downregulate the expression of HIF-1α, an important nuclear transcription regulation factor adapting hypoxia . The RA synovial cells with tumor-like proliferation and massive inflammatory cell infiltration increase oxygen consumption, resulting in local hypoxia of the RA inflammatory joints .…”

Section: Results and Discussionsupporting

confidence: 56%

“…Therefore, we confirmed by in vitro experiments that the CuAP could effectively scavenge ROS, ameliorate hypoxia in cells, and downregulate the expression of HIF-1α, an important nuclear transcription regulation factor adapting hypoxia. 46 The RA synovial cells with tumor-like proliferation and massive inflammatory cell infiltration increase oxygen consumption, resulting in local hypoxia of the RA inflammatory joints. 47 At this time, HIF-1α expression is upregulated, promoting the development of RA.…”

Section: ■ Introductionmentioning

confidence: 99%

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Polymerized Network-Based Artificial Peroxisome Reprogramming Macrophages for Photoacoustic Imaging-Guided Treatment of Rheumatoid Arthritis

Wang,

Zhang,

Chen

et al. 2024

ACS Appl. Mater. Interfaces

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Artificial peroxisomes (AP) with enzyme-mimetic catalytic activity and recruitment ability have drawn a great deal of attention in fabricating protocell systems for scavenging reactive oxygen species (ROS), modulating the inflammatory microenvironment, and reprogramming macrophages, which is of great potential in treating inflammatory diseases such as rheumatoid arthritis (RA). Herein, a macrophage membrane-cloaked Cu-coordinated polyphthalocyanine-based AP (CuAP) is prepared with a macrocyclic conjugated polymerized network and embedded Cu-single atomic active center, which mimics the catalytic activity and coordination environment of natural superoxide dismutase and catalase, possesses the inflammatory recruitment ability of macrophages, and performs photoacoustic imaging (PAI)-guided treatment. The results of both in vitro cellular and in vivo animal experiments demonstrated that the CuAP under ultrasound and microbubbles could efficiently scavenge excess ROS in cells and tissues, modulate microenvironmental inflammatory cytokines such as interleukin-1β, tumor necrosis factor-α, and arginase-1, and reprogram macrophages by polarization of M1 (proinflammatory phenotype) to M2 (anti-inflammatory phenotype). We believe this study offers a proof of concept for engineering multifaceted AP and a promising approach for a PAI-guided treatment platform for RA.

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Section: Results and Discussionsupporting

confidence: 56%

Section: ■ Introductionmentioning

confidence: 99%

Polymerized Network-Based Artificial Peroxisome Reprogramming Macrophages for Photoacoustic Imaging-Guided Treatment of Rheumatoid Arthritis

Wang,

Zhang,

Chen

et al. 2024

ACS Appl. Mater. Interfaces

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“…However, it has been proposed that in vivo hypoxia promotes HIF-1α accumulation, and elevated HIF-1α expression promotes macrophage M1 polarization through activation of the HIF-1α/pyruvate kinase M2 (PKM2) axis. 32 This suggests that there may be more complex regulatory pathways for macrophage response to hypoxic stimuli in our body. More importantly, hypoxia is not a binary phenomenon.…”

Section: Discussionmentioning

confidence: 99%

Macrophage M2 polarization promotes pulpal inflammation resolution during orthodontic tooth movement

Li,

Ren,

Zhang

et al. 2024

J Cellular Molecular Medi

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Mechanical force induces hypoxia in the pulpal area by compressing the apical blood vessels of the pulp, triggering pulpal inflammation during orthodontic tooth movement. However, this inflammation tends to be restorable. Macrophages are recognized as pivotal immunoreactive cells in the dental pulp. Whether they are involved in the resolution of pulpal inflammation in orthodontic teeth remains unclear. In this study, we investigated macrophage polarization and its effects during orthodontic tooth movement. It was demonstrated that macrophages within the dental pulp polarized to M2 type and actively participated in the process of pulpal inflammation resolution. Inflammatory reactions were generated and vascularization occurred in the pulp during orthodontic tooth movement. Macrophages in orthodontic pulp show a tendency to polarize towards M2 type as a result of pulpal hypoxia. Furthermore, by blocking M2 polarization, we found that macrophage M2 polarization inhibits dental pulp‐secreting inflammatory factors and enhances VEGF production. In conclusion, our findings suggest that macrophages promote pulpal inflammation resolution by enhancing M2 polarization and maintaining dental health during orthodontic tooth movement.

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“…In AF, an up-regulation of the hypoxia-inducible factor (HIF) pathway and an increased expression of hypoxic and angiogenic markers were observed [49], and the transcription factor HIF-1α is upregulated in the adipose tissue in obesity. In obesity, HIF-1α contributes to chronic inflammation by promoting the expression of proinflammatory cytokines and recruiting M1 macrophages [50]. The increased expression of HIF-1α leads to the activation of a profibrotic transcriptional program, resulting in collagen I, III, IV, and lysyl oxidase synthesis, ultimately causing fibrosis in the adipose tissue [51,52].…”

Section: Inflammation In Obesity and Atrial Fibrillationmentioning

confidence: 99%

Oxidative Stress, Inflammation, and Mitochondrial Dysfunction: A Link between Obesity and Atrial Fibrillation

Balan,

Halațiu,

Scridon

2024

Antioxidants

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The adipose tissue has long been thought to represent a passive source of triglycerides and fatty acids. However, extensive data have demonstrated that the adipose tissue is also a major endocrine organ that directly or indirectly affects the physiological functions of almost all cell types. Obesity is recognized as a risk factor for multiple systemic conditions, including metabolic syndrome, type 2 diabetes mellitus, sleep apnea, cardiovascular disorders, and many others. Obesity-related changes in the adipose tissue induce functional and structural changes in cardiac myocytes, promoting a wide range of cardiovascular disorders, including atrial fibrillation (AF). Due to the wealth of epidemiologic data linking AF to obesity, the mechanisms underlying AF occurrence in obese patients are an area of rich ongoing investigation. However, progress has been somewhat slowed by the complex phenotypes of both obesity and AF. The triad inflammation, oxidative stress, and mitochondrial dysfunction are critical for AF pathogenesis in the setting of obesity via multiple structural and functional proarrhythmic changes at the level of the atria. The aim of this paper is to provide a comprehensive view of the close relationship between obesity-induced oxidative stress, inflammation, and mitochondrial dysfunction and the pathogenesis of AF. The clinical implications of these mechanistic insights are also discussed.

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Hypoxia inducible factor-1α is an important regulator of macrophage biology

Cited by 12 publications

References 73 publications

Polymerized Network-Based Artificial Peroxisome Reprogramming Macrophages for Photoacoustic Imaging-Guided Treatment of Rheumatoid Arthritis

Polymerized Network-Based Artificial Peroxisome Reprogramming Macrophages for Photoacoustic Imaging-Guided Treatment of Rheumatoid Arthritis

Macrophage M2 polarization promotes pulpal inflammation resolution during orthodontic tooth movement

Oxidative Stress, Inflammation, and Mitochondrial Dysfunction: A Link between Obesity and Atrial Fibrillation

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