The basic helix-loop-helix transcription factor scleraxis (Scx) is overexpressed in systemic and lung fibrosing diseases

Mendoza-Milla, Criselda; Machorro, Ana Lilia Torres; Castillo, Gael Guitrón; Rodríguez‐Reyna, Tatiana Sofía; Ramos, Joaquín Zúñiga; Roldán, Ivette Buendia

doi:10.1183/1393003.congress-2017.pa895

Cited by 1 publication

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“…Scleraxis expression increases in healing bone fractures, and scleraxis null mice exhibit a significant impairment in callus formation resulting in defective healing of fractures [71]. Conversely, elevated scleraxis expression has been noted in collagen-rich dermal keloids, and has been detected at elevated levels in the serum of patients with systemic sclerosis or idiopathic pulmonary fibrosis compared to healthy controls [72,73]. It is tempting to speculate, therefore, that scleraxis represents a key effector of wound healing pathways in multiple tissues, controlling the activation of fibroblasts to facilitate healing, and that its potential role in fibrosis stems from the excessive or prolonged activation of these pathways.…”

Section: Fibroblast To Myofibroblast Phenotype Conversionmentioning

confidence: 99%

Cardiac Fibroblast to Myofibroblast Phenotype Conversion—An Unexploited Therapeutic Target

Czubryt

2019

JCDD

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Fibrosis occurs when the synthesis of extracellular matrix outpaces its degradation, and over time can negatively impact tissue and organ function. In the case of cardiac fibrosis, contraction and relaxation of the heart can be impaired to the point of precipitating heart failure, while at the same time fibrosis can result in arrhythmias due to altered electrical properties of the myocardium. The critical event in the evolution of cardiac fibrosis is the phenotype conversion of cardiac fibroblasts to their overly-active counterparts, myofibroblasts: cells demarked by their expression of novel markers such as periostin, by their gain of contractile activity, and by their pronounced and prolonged increase in the production of extracellular matrix components such as collagens. The phenotype change is dramatic, and can be triggered by many stimuli, including mechanical force, inflammatory cytokines, and growth factors. This review will explore fibroblast to myofibroblast transition mechanisms and will consider the therapeutic potential of targeting this process as a means to arrest or even reverse cardiac fibrosis.

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Section: Fibroblast To Myofibroblast Phenotype Conversionmentioning

confidence: 99%

Cardiac Fibroblast to Myofibroblast Phenotype Conversion—An Unexploited Therapeutic Target

Czubryt

2019

JCDD

View full text Add to dashboard Cite

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The basic helix-loop-helix transcription factor scleraxis (Scx) is overexpressed in systemic and lung fibrosing diseases

Cited by 1 publication

References 0 publications

Cardiac Fibroblast to Myofibroblast Phenotype Conversion—An Unexploited Therapeutic Target

Cardiac Fibroblast to Myofibroblast Phenotype Conversion—An Unexploited Therapeutic Target

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