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Molecular adaptations to endurance exercise and skeletal muscle fibre plasticity
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
To summarise, PGC-1α increases the expression of VEGF and other growth factors that stimulate angiogenesis following exercise by co-activating ERRα. VEGF appears to be the master regulator of angiogenesis, and as such, regulates the proliferation, migration, elongation, network formation, branching and leakiness of endothelial cells. HIF-1α stabilisation can increase mitochondrial mass in response to low PO2; however, this does not seem to be necessary for the exercise-induced increase in capillaries. One could hypothesise that HIF-1α plays a role in increasing mitochondrial mass at altitude; however, while there is a transient increase in VEGF at altitude, there is no increase in capillaries in response to eight weeks at 4,100 m, and individuals who are native to 4,100 m altitude show normal VEGF levels and FEWER capillaries per muscle fibre (93). Together, these data suggest that HIF-1α contributes to baseline capillary density in muscle, whereas exercise increases capillaries in a PGC-1α-ERRα-dependent manner.
Age-Related Macular Degeneration
Published in Ching-Yu Cheng, Tien Yin Wong, Ophthalmic Epidemiology, 2022
Jost B. Jonas, Songhomitra Panda-Jonas
Interestingly, the number of persons being blind due to AMD decreased slightly from 1990 (2.2 million; 80% UI: 0.2–8.3 million) to 2015 (2.0 million; 80% UI: 0.2–7.3 million), and the number of persons with AMD-related MSVI also decreased slightly from 1990 (8.5 million; 80% UI: 1.0–29.4 million) to 2015 (8.4 million; 80% UI: 0.9–29.5 million).77 Since during the same period global population increased by >30%, the decrease in the number of individuals affected by AMD-related blindness and MSVI corresponded to a decrease in the age-adjusted prevalence of AMD-related blindness and AMD-related MSVI. The slight reduction in the total number of individuals affected by AMD-related blindness or AMD-related MSVI is even more remarkable if one takes into account the worldwide demographic transition with a substantial increase in the average age in most regions and falling death rates.78 Since the drop in the age-standardized prevalence of macular degeneration-related blindness took place mostly in high-income regions, one may infer that it was due to the clinical introduction of intravitreally applied anti-VEGF drugs.50–53 The reduction in the age-standardized prevalence of macular degeneration-related blindness was markedly less profound than the global decrease in the age-standardized prevalence of blindness due to cataract, under-corrected refractive error, and trachoma.35,76,77
Approach to Retinal Vascular Disease
Published in Anita Prasad, Laser Techniques in Ophthalmology, 2022
Anti-VEGF treatment, though effective, needs frequent monitoring and re-treatment, with potential ocular and systemic side-effects with each treatment. IVT can cause decreased retinal perfusion, CR atrophy, and TRD in patients with florid PDR. The ongoing nature of treatment leads to increased socio-economic costs and medical burden.
Endothelial progenitor cells promote neural stem cell proliferation in hypoxic conditions through VEGF via the PI3K/AKT pathway
Published in Journal of Receptors and Signal Transduction, 2022
Jingti Jing, Haoming Jiang, Lin Zhang
Our results demonstrate that EPCs cultured in hypoxic conditions for 24 h could secrete VEGF as reported by Leung, et al. VEGF is a growth factor with the main function of angiogenesis promotion [9]. Emerging evidences suggest that VEGF plays a pivotal role in the recovery of many central nervous system disorders, such as cerebral ischemia, Alzheimer’s disease, Parkinson’s disease, etc. Besides its role in blood vessel growth, VEGF has also been shown to participate in neurogenesis. Several studies have recently reported that both the injured spinal cord and cultured neural stem cells express VEGF and its receptors and that VEGF stimulates neurogenesis in vivo and in vitro [12,13]. VEGF isoforms and its receptors have been identified in the primary culture of NSCs grown as neurospheres [14]. Exogenous VEGF promotes the proliferation of neural stem cells in vitro via VEGF binding to VEGFR-2, whereas this effect can be blocked by VEGFR-2 inhibitors [15]. Release of VEGF into culture medium and the presence of VEGFR-2 indicate an autocrine mechanism for VEGF signaling during neural stem cell expansion [15]. The mechanism of VEGF in neurogenesis is not well understood and some researchers have suggested that the effect of VEGF on neurogenesis involves the PI3/Akt and Ras/Raf/MEK/ERK signaling pathways [16,17]. In our study, we demonstrated that the effect of VEGF mediated promotion of NSC proliferation involves the PI3/AKT signaling pathway.
The effects of microRNA-126 reduced inflammation and apoptosis of diabetic nephropathy through PI3K/AKT signalling pathway by VEGF
Published in Archives of Physiology and Biochemistry, 2022
Zhe Lou, Qiaobei Li, Chunyan Wang, Yinyan Li
Vascular endothelial growth factor (VEGF) is a mitosis-stimulating factor and chemokine of endothelial cell (Isner et al.2001). It targets vascular endothelial cell, the important source of VEGF (Isner et al. 2001). VEGF plays an important regulatory role in physiological angiogenesis and pathological revascularisation (Miaomiao et al.2016). It possesses multiple functions, such as promoting revascularisation, increasing vascular permeability and protecting neuron. During wound repair, VEGF can stimulate endothelial cell growth and promote wound vascularisation (Amoli et al. 2011). As is indicated in clinical and animal experiments, the VEGF gene expression level in skeletal muscle in DF patients are remarkably lower than that in patients with non-diabetic lower limb atherosclerosis and occlusion (Amoli et al. 2011). Expression levels of VEGF on wound surface of diabetic rats at all time points after injury are notably lower than those in normal control rats. Reduced VEGF gene expression in the ischaemic limb will result in notably reduced collateral vessels around the occlusive vessels in DN (Miaomiao et al. 2016). Thus, it leads to insufficient collateral compensation and persistent progression of ischaemic ulcer that can hardly heal. It may account for an important cause of ulcer in DN (Miaomiao et al. 2016).
An appraisal of vascular endothelial growth factor (VEGF): the dynamic molecule of wound healing and its current clinical applications
Published in Growth Factors, 2022
Aakansha Giri Goswami, Somprakas Basu, Farhanul Huda, Jayanti Pant, Amrita Ghosh Kar, Tuhina Banerjee, Vijay Kumar Shukla
VEGF is one of the important growth factors involved in angiogenesis and tissue repair in wound healing. It coordinates multiple events in angiogenesis including vasodilation, endothelial migration, and neo-angiogenesis in the growing tissue. It also links the inflammatory and proliferation phase of wound healing and induces cell-to-cell crosstalk at different phases of wound healing. Absence of VEGF and its receptors or their inhibition adversely affect wound healing and leads to poor granulation tissue formation. For its unique function of coordination of various cellular mechanisms and its ubiquitous presence in the wound bed throughout healing, it has been used in laboratory and in trials in diabetic, venous, ischemic, and pressure ulcers. When compared with other growth factors involved in wound healing, few attempts have been made to use VEGF clinically as an adjunctive treatment in wound healing. Clinical studies on gene transfer had very limited success in intramuscular use of VEGF165 to treat nonhealing, ischemic ulcers. Despite encouraging studies in animal models, no topically based VEGF preparation has been reported in clinical use even after a number of human trials. Although current reports suggest limiting its use, better understanding of its complex mechanism of action, and hence manipulating its use such as in sustained delivery platforms, may yield encouraging results in hard-to-heal wounds in future.