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Details for anatomical structure: smooth muscle

EndoNet ID: ENC00128

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smooth muscle, ,

Links to other resources

Cytomer cy0041805

Larger structures

  • muscle


  • smooth_muscle_cell

Secreted hormones

  • Hormone: pentraxin 3

    • PTX3 is produced by different cell types of the vessel wall, including SMCs. [1]
    • Modified atherogenic lipoproteins induce expression of pentraxin-3 by human vascular smooth muscle cells. [2]
  • Hormone: PDGFD

  • Hormone: eotaxin

    • Human eotaxin is an 8,3-kDa, 74-amino-acid residue, nonglycosylated polypeptide secreted by endothelial cells, fibroblasts, macrophages, ciliated and nonciliated bronchial epithelial cells, smooth muscle cells, chondrocytes, and eosinophils. [3]
  • Hormone: galectin-1

  • Hormone: galectin-1

  • Hormone: EGF

  • Hormone: FGF-1 isoform 1

  • Hormone: VCAM1 soluble form

  • Hormone: 20-HETE


  • Receptor: NPY5-R

  • Receptor: PPARgamma1

    • The peroxisome proliferation-activated receptor gamma (PPAR╬│)1 is a member of the nuclear receptor superfamily. It is expressed in many cell types, including adipocytes, epithelial cells, B- and T-cells, macrophages, endothelial cells, neutrophils, and smooth muscle cells [4]
  • Receptor: ER-beta

    Induced phenotype:

    • vascular smooth muscle cell development
      • Estradiol is a potent inhibitor of vascular smooth muscle cell growth. [5]
      • Estradiol stimulates cAMP synthesis and cAMP-derived adenosine regulates smooth muscle cell growth via A(2) adenosine receptors. This cAMP-adenosine pathway may contribute to the antivasooclusive effects of estradiol. [5]
  • Receptor: T-cadherin

  • Receptor: CysLTR2

  • Receptor: TNFRSF12A

    Induced phenotype:

    • positive regulation of smooth muscle proliferation
      • TNFSF12 induces proliferation of human aortic smooth muscle cells in vitro. [6]
  • Receptor: CCK-2

  • Receptor: TrpV4-A

    Induced phenotype:

    • positive regulation of smooth muscle contraction
      • Functional TRPV4 is expressed in human airway smooth muscle cells and may act as an osmolarity sensor in the airway. [7]
      • Activation of TRPV4 on airway smooth muscle cells increases intracellular Ca2+ level, which may induce smooth muscle contraction. [7]
      • TRPV4 is the most plausible channel involved in hypotonic stimulation-induced airway contraction. [7]
  • Receptor: Vascular endothelial growth factor receptor 1

    • These findings demonstrate that vascular SMCs express functional flt-1 receptors after arterial injury. [8]

    Induced phenotype:

    • vessel maturation
      • PlGF also acts on VEGFR-1-expressing smooth muscle cells, thus promoting vessel maturation. [9]