The Role of Tenascin C in Cardiac Reverse Remodeling Following Banding-Debanding of the Ascending Aorta.
Mireia Perera-GonzalezAttila KissPhilipp KaiserMichael HolzweberFelix NagelSimon WatzingerEylem AcarPetra Lujza SzaboInês Fonseca GonçalvesLukas WeberPatrick Michael PilzLubos BudinskyThomas H HelbichBruno Karl PodesserPublished in: International journal of molecular sciences (2021)
Pressure overload, when lasting long enough to induce HF, has less potential for reverse remodeling in mice. This may be due to significant upregulation of TN-C expression, which stimulates ACE 1, Col 1, and alpha-smooth muscle actin (α-SMA) upregulation in fibroblasts. Consequently, addressing TN-C in LV hypertrophy might open a new window for future therapeutics.
Keyphrases
- smooth muscle
- poor prognosis
- long non coding rna
- pulmonary artery
- cell proliferation
- minimally invasive
- signaling pathway
- left ventricular
- aortic valve
- aortic dissection
- current status
- high fat diet induced
- pulmonary hypertension
- coronary artery
- angiotensin converting enzyme
- adipose tissue
- binding protein
- pulmonary arterial hypertension
- metabolic syndrome
- risk assessment
- cell migration