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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
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  4. Monthly Traffic Estimate
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We began analyzing https://link.springer.com/article/10.1007/s43032-022-01064-0, but it redirected us to https://link.springer.com/article/10.1007/s43032-022-01064-0. The analysis below is for the second page.

Title[redir]:
Importance of Fibrosis in the Pathogenesis of Uterine Leiomyoma and the Promising Anti-fibrotic Effects of Dipeptidyl Peptidase-4 and Fibroblast Activation Protein Inhibitors in the Treatment of Uterine Leiomyoma | Reproductive Sciences
Description:
Uterine fibroid or leiomyoma is the most common benign uterus tumor. The tumor is primarily composed of smooth muscle (fibroid) cells, myofibroblast, and a significant amount of extracellular matrix components. It mainly affects women of reproductive age. They are uncommon before menarche and usually disappear after menopause. The fibroids have excessive extracellular matrix components secreted by activated fibroblast cells (myofibroblast). Myofibroblast has the characteristics of fibroblast and smooth muscle cells. These cells possess contractile capability due to the expression of contractile proteins which are normally found only in muscle tissues. The rigid nature of the tumor is responsible for many side effects associated with uterine fibroids. The current drug treatment strategies are primarily hormone-driven and not anti-fibrotic. This paper emphasizes the fibrotic background of uterine fibroids and the mechanisms behind the deposition of excessive extracellular matrix components. The transforming growth factor-β, hippo, and focal adhesion kinase-mediated signaling pathways activate the fibroblast cells and deposit excessive extracellular matrix materials. We also exemplify how dipeptidyl peptidase-4 and fibroblast activation protein inhibitors could be beneficial in reducing the fibrotic process in leiomyoma. Dipeptidyl peptidase-4 and fibroblast activation protein inhibitors prevent the fibrotic process in organs such as the kidneys, lungs, liver, and heart. These inhibitors are proven to inhibit the signaling pathways mentioned above at various stages of their activation. Based on literature evidence, we constructed a narrative review on the mechanisms that support the beneficial effects of dipeptidyl peptidase-4 and fibroblast activation protein inhibitors for treating uterine fibroids.

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

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Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


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How Does Doi.org Make Money? {💸}

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Keywords {🔍}

pubmed, article, google, scholar, cas, central, uterine, activation, cell, fibroblast, fibroids, growth, transforming, cancer, protein, signaling, leiomyoma, biol, fibrosis, peptidase, matrix, dipeptidyl, cells, httpsdoiorgs, res, tgfβ, factorβ, med, fibroid, extracellular, expression, receptor, treatment, tumor, human, proliferation, mol, effects, inhibitors, reprod, obstet, httpsdoiorg, sci, clin, factor, fibroblasts, liu, pathways, gynecol, int,

Topics {✒️}

month download article/chapter latent tgf-β-binding protein-1 transforming growth factor-β rho/rock–dependent signaling pathways transforming growth factor-β3 transforming growth factor-β1 tgf-β/smad signaling system fibroblast activation protein-α fibroblast activation protein-alpha lipopolysaccharide-induced lung injury receptor kinase-independent manner regulates tgf-β stimulation tgf-β-activated kinase-1 wnt/β-catenin pathway latent tgf-β structure keloid-derived skin fibroblasts α-smooth muscle actin tgf-βreceptor kinase activity fibroblast-mediated matrix contraction gly-x-gly interruptions streptozotocin-induced diabetic mice emdormi rymbai full article pdf fibroblast activation protein promising anti-fibrotic effects augments progesterone signaling fibroid cell proliferation de oliveira mf stromal fibroblast activation tgf-β signaling uterine fibroid cells smooth muscle cells uterine fibroid etiology uterine fibroid symptoms 1007/s43032-019-00106-4 cd26/dipeptidyl peptidase-4 dipeptidyl peptidase iv dipeptidyl peptidase-4 inhibitors dipeptidyl peptidase iv estrogen-mediated activation rho-rock signaling ras-erk signaling plasminogen activator system vascular smooth muscle privacy choices/manage cookies uterine fibroid biology cell commun signal placebo-controlled multicenter study islam ms hamson ej

Questions {❓}

  • Fibroblast activation protein-α in fibrogenic disorders and cancer: more than a prolyl-specific peptidase?
  • Medical therapy for fibroids: what next for ulipristal acetate?
  • Resistance to transforming growth factor β-mediated tumor suppression in melanoma: are multiple mechanisms in place?
  • Uterine fibroids - What’s new?

Schema {🗺️}

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         description:Uterine fibroid or leiomyoma is the most common benign uterus tumor. The tumor is primarily composed of smooth muscle (fibroid) cells, myofibroblast, and a significant amount of extracellular matrix components. It mainly affects women of reproductive age. They are uncommon before menarche and usually disappear after menopause. The fibroids have excessive extracellular matrix components secreted by activated fibroblast cells (myofibroblast). Myofibroblast has the characteristics of fibroblast and smooth muscle cells. These cells possess contractile capability due to the expression of contractile proteins which are normally found only in muscle tissues. The rigid nature of the tumor is responsible for many side effects associated with uterine fibroids. The current drug treatment strategies are primarily hormone-driven and not anti-fibrotic. This paper emphasizes the fibrotic background of uterine fibroids and the mechanisms behind the deposition of excessive extracellular matrix components. The transforming growth factor-β, hippo, and focal adhesion kinase-mediated signaling pathways activate the fibroblast cells and deposit excessive extracellular matrix materials. We also exemplify how dipeptidyl peptidase-4 and fibroblast activation protein inhibitors could be beneficial in reducing the fibrotic process in leiomyoma. Dipeptidyl peptidase-4 and fibroblast activation protein inhibitors prevent the fibrotic process in organs such as the kidneys, lungs, liver, and heart. These inhibitors are proven to inhibit the signaling pathways mentioned above at various stages of their activation. Based on literature evidence, we constructed a narrative review on the mechanisms that support the beneficial effects of dipeptidyl peptidase-4 and fibroblast activation protein inhibitors for treating uterine fibroids.
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      headline:Importance of Fibrosis in the Pathogenesis of Uterine Leiomyoma and the Promising Anti-fibrotic Effects of Dipeptidyl Peptidase-4 and Fibroblast Activation Protein Inhibitors in the Treatment of Uterine Leiomyoma
      description:Uterine fibroid or leiomyoma is the most common benign uterus tumor. The tumor is primarily composed of smooth muscle (fibroid) cells, myofibroblast, and a significant amount of extracellular matrix components. It mainly affects women of reproductive age. They are uncommon before menarche and usually disappear after menopause. The fibroids have excessive extracellular matrix components secreted by activated fibroblast cells (myofibroblast). Myofibroblast has the characteristics of fibroblast and smooth muscle cells. These cells possess contractile capability due to the expression of contractile proteins which are normally found only in muscle tissues. The rigid nature of the tumor is responsible for many side effects associated with uterine fibroids. The current drug treatment strategies are primarily hormone-driven and not anti-fibrotic. This paper emphasizes the fibrotic background of uterine fibroids and the mechanisms behind the deposition of excessive extracellular matrix components. The transforming growth factor-β, hippo, and focal adhesion kinase-mediated signaling pathways activate the fibroblast cells and deposit excessive extracellular matrix materials. We also exemplify how dipeptidyl peptidase-4 and fibroblast activation protein inhibitors could be beneficial in reducing the fibrotic process in leiomyoma. Dipeptidyl peptidase-4 and fibroblast activation protein inhibitors prevent the fibrotic process in organs such as the kidneys, lungs, liver, and heart. These inhibitors are proven to inhibit the signaling pathways mentioned above at various stages of their activation. Based on literature evidence, we constructed a narrative review on the mechanisms that support the beneficial effects of dipeptidyl peptidase-4 and fibroblast activation protein inhibitors for treating uterine fibroids.
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         Transforming growth factor-β
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         Leiomyoma
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         Embryology
         Obstetrics/Perinatology/Midwifery
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