Pioglitazone‐induced myofibroblast cell death: implications for cutaneous scarring

  title={Pioglitazone‐induced myofibroblast cell death: implications for cutaneous scarring},
  author={Ronan O'Leary and Sreenivasan Ponnambalam and Edward J. Wood},
  journal={British Journal of Dermatology},
Wound healing potential of scaffolds prepared from porcine jejunum and urinary bladder by a non-detergent/enzymatic method
The results suggested that JDS and UDS prepared by non-detergent/enzymatic method have potential clinical applications and induced higher cell proliferation and greater angiogenesis than UDS probably indicating better healing by the former.
Rosiglitazone modulates the behaviors of diabetic host‐derived fibroblasts in a carboxymethyllysine‐modified collagen model
  • Huijuan Liao, I. Pastar, Weiliam Chen
  • Biology
    Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
  • 2012
Rosiglitazone induced fibroblast migration, α‐smooth muscle actin production, and transformation into myofibroblasts in the presence of advanced glycation end products, and its potential as a topical treatment of diabetic chronic wounds is identified.
Rosiglitazone increases matrix production and quenches inflammation: studies in human cells
The effect of therapeutic doses of rosiglitazone on proliferative and inflammatory pathways in fibroblasts (HF) from five controls and five T2D patients, and in aortic smooth muscle cells (hSMC) is tested.
Thiazolidinediones in dermatology
  • A. Boyd
  • Medicine, Biology
    International journal of dermatology
  • 2007
Clinicians should become familiar with glitazones as they are experiencing a burgeoning use among patients with non‐insulin‐dependent diabetes mellitus and have demonstrated clinical efficacy in treating certain skin conditions.
Author index
  • Medicine
  • 2003
The IgA and IgG response to the epidermal antigens demonstrates that intermolecular epitope spreading is associated with IgA rather than IgG antibodies, and is more common in adults than in children.


Thiazolidinediones: A pharmacological overview
The pharmacodynamic and clinical profiles of the thiazolidinediones suggest that they may positively influence the processes that contribute to the development of type 2 diabetes mellitus and other disorders of insulin resistance.
Pioglitazone prevents early-phase hepatic fibrogenesis caused by carbon tetrachloride.
In conclusion, pioglitazone inhibits both hepatic inflammation and activation of hepatic stellate cells, thereby ameliorating early-phase fibrogenesis in the liver following acute CCl(4).
Peroxisome proliferator-activated receptor-beta signaling contributes to enhanced proliferation of hepatic stellate cells.
PPAR-beta is an important signal-transducing factor contributing to hepatic stellate cell proliferation during acute and chronic liver inflammation.
Antidiabetic thiazolidinediones inhibit collagen synthesis and hepatic stellate cell activation in vivo and in vitro.
Oral administration of TZD reduced extracellular matrix deposition and HSC activation in both toxic and cholestatic models of liver fibrosis, indicating that PPARgamma activation in HSC retards fibrosis in vivo and suggest the use of TzD for the treatment of Liver fibrosis.
Apoptosis mediates the decrease in cellularity during the transition between granulation tissue and scar.
The results indicate that the number of myofibroblastic and vascular cells undergoing apoptosis increases as the wound closes and support the assumption that this is the mechanism of granulation tissue evolution into a scar.
Glitazones: clinical effects and molecular mechanisms
In summary, with the thiazolidinediones a novel concept for the treatment of insulin resistance is available that in theory could also be used for prevention of type 2 diabetes.
Myofibroblasts and mechano-regulation of connective tissue remodelling
It is clear that the understanding of the myofibroblast — its origins, functions and molecular regulation — will have a profound influence on the future effectiveness not only of tissue engineering but also of regenerative medicine generally.
Transforming growth factor-beta 1 induces alpha-smooth muscle actin expression in granulation tissue myofibroblasts and in quiescent and growing cultured fibroblasts
It is shown that the subcutaneous administration of transforming growth factor- beta 1 to rats results in the formation of a granulation tissue in which alpha-SM actin expressing myofibroblasts are particularly abundant, suggesting that TGF beta 1 plays an important role in my ofibroblast differentiation during wound healing and fibrocontractive diseases by regulating the expression of alpha- SM actin in these cells.