rhFGF20 promotes angiogenesis and vascular repair following traumatic brain injury by regulating Wnt/β-catenin pathway

Guo, Ruili; Wang, Xue; Fang, Yani; Chen, Xiongjian; Chen, Kun; Huang, Wenting; Hu, Jian; Liang, Fei; Du, Jingting; Dordoe, Confidence; Tian, Xianxi; Lin, Li

doi:10.1016/j.biopha.2021.112200

Cited by 20 publications

(13 citation statements)

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“…TBI stands as a primary cause of long-term disabilities among adolescents [ 31 ]. Worldwide, around 70 million individuals experience TBI annually, with treatment costs exceeding $400 billion [ 29 , 32 ], posing a substantial challenge to socio-economic realms and posing a weighty public health concern [ 7 ]. From the perspectives of pathology and etiology, one of the principal complications accompanying therapeutic approaches to traumatic brain injuries is the intricacy of their underlying mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Transcranial direct current stimulation promotes angiogenesis and improves neurological function via the OXA-TF-AKT/ERK signaling pathway in traumatic brain injury

Ren,

Kang,

Wang

et al. 2024

Aging

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Traumatic brain injury (TBI) and its resulting complications pose a major challenge to global public health, resulting in increased rates of disability and mortality. Cerebrovascular dysfunction is nearly universal in TBI cases and is closely associated with secondary injury after TBI. Transcranial direct current stimulation (tDCS) shows great potential in the treatment of TBI; however, the exact mechanism remains elusive. In this study, we performed in vivo and in vitro experiments to explore the effects and mechanisms of tDCS in a controlled cortical impact (CCI) rat model simulating TBI. In vivo experiments show that tDCS can effectively reduce brain tissue damage, cerebral edema and neurological deficits. The potential mechanism may be that tDCS improves the neurological function of rats by increasing orexin A (OXA) secretion, upregulating the TF-AKT/ERK signaling pathway, and promoting angiogenesis at the injury site. Cellular experiments showed that OXA promoted HUVEC migration and angiogenesis, and these effects were counteracted by the ERK1/2 inhibitor LY3214996. The results of Matrigel experiment in vivo showed that TNF-a significantly reduced the ability of HUVEC to form blood vessels, but OXA could rescue the effect of TNF-a on the ability of HUVEC to form blood vessels. However, LY3214996 could inhibit the therapeutic effect of OXA. In summary, our preliminary study demonstrates that tDCS can induce angiogenesis through the OXA-TF-AKT/ERK signaling pathway, thereby improving neurological function in rats with TBI.

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Section: Discussionmentioning

confidence: 99%

Transcranial direct current stimulation promotes angiogenesis and improves neurological function via the OXA-TF-AKT/ERK signaling pathway in traumatic brain injury

Ren,

Kang,

Wang

et al. 2024

Aging

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“…Additionally, the pathway facilitates the accumulation of β-catenin, a vital transcriptional co-activator, within the nucleus of cells. [71] This accumulation initiates the expression of genes that increase osteoblast activity, leading to accelerated bone healing.…”

Section: Wnt/β-catenin Pathwaymentioning

confidence: 99%

“…The activation of the Wnt/β-catenin pathway post-TBI accelerates bone healing and promotes osteoblast activity. [71] The osteoblasts then search for new bone tissue with high precision. By capitalizing on the innate regenerative potential of the Wnt/β-catenin pathway, TBIs enable the rapid and efficient recovery of injured bone, reestablishing its structural integrity and function.…”

Section: Wnt/β-catenin Pathwaymentioning

confidence: 99%

“…At the molecular level, the Wnt/β‐catenin pathway exerts its influence by regulating the expression of osteogenic genes, ensuring their optimal function in bone healing. Additionally, the pathway facilitates the accumulation of β‐catenin, a vital transcriptional co‐activator, within the nucleus of cells [71] . This accumulation initiates the expression of genes that increase osteoblast activity, leading to accelerated bone healing.…”

Section: Signaling Pathways In Tbi‐induced Bone Healingmentioning

confidence: 99%

“…The activation of the Wnt/β‐catenin pathway post‐TBI accelerates bone healing and promotes osteoblast activity [71] . The osteoblasts then search for new bone tissue with high precision.…”

Section: Signaling Pathways In Tbi‐induced Bone Healingmentioning

confidence: 99%

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The mechanism of bone healing after traumatic brain injury

Xiong,

Zhong,

2023

Brain-X

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A growing body of evidence suggests that patients who experience traumatic brain injuries (TBIs) exhibit significantly shorter healing periods compared to those with isolated fractures. However, the precise underlying mechanism behind this phenomenon remains unclear. Recent studies have shed light on the potential role of hormonal signals and neural circuits originating in the hypothalamus, which play vital roles in regulating the skeletal system. Despite these advances, there is a lack of comprehensive research summarizing the crucial role of bone healing in TBIs and the underlying mechanisms. This review aimed to explore the underlying mechanisms responsible for the accelerated bone healing observed in TBI patients, with a specific focus on the intricate crosstalk between TBI and bone remodeling. Additionally, we comprehensively discuss and summarize the beneficial effects of TBI on the skeletal system and examine the TBI‐induced signaling pathways that result in accelerated fracture healing and bone remodeling. By dissecting these pathways, we aim to identify potential targets for intervention and bone repair promotion.

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