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AXL receptor tyrosine kinase is increased in patients with heart failure
M Batlle1, P Recarte-Pelz2, E Roig3
1Biomedical Research Institute August Pi i Sunyer (IDIBAPS), Spain; Thorax Institute, Cardiology Department, Hospital Clínic de Barcelona, Spain.
Insights
AXL receptor tyrosine kinase is elevated in heart failure (HF) patients. Higher soluble AXL (sAXL) levels predict major HF events, suggesting a new pathway in myocardial damage independent of BNP.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biomarker Discovery
Background:
- AXL, a receptor tyrosine kinase, is highly expressed in the heart and plays a role in cardiovascular physiology.
- The specific role of AXL in heart failure (HF) has not been previously investigated.
Purpose of the Study:
- To investigate the expression and clinical significance of AXL in patients with heart failure.
- To determine if soluble AXL (sAXL) can serve as a biomarker for HF progression and prognosis.
Main Methods:
- Quantified myocardial AXL protein expression in end-stage HF patients versus controls.
- Measured serum sAXL and B-type natriuretic peptide (BNP) levels in a cohort of chronic HF patients and controls.
- Analyzed clinical data, demographic information, and patient outcomes including mortality and HF hospitalizations.
Main Results:
- AXL protein expression was significantly elevated (6-fold) in myocardial biopsies of HF patients compared to controls.
- Serum sAXL levels were higher in HF patients (86.3 ng/mL) than in controls (67.8 ng/mL).
- Elevated sAXL levels correlated with parameters of worse HF prognosis and predicted major HF events within one year, independent of BNP levels.
Conclusions:
- Both myocardial and serum AXL levels are elevated in HF patients.
- Peripheral sAXL is associated with HF progression and predicts adverse events, suggesting its potential as a novel biomarker.
- sAXL may represent a new molecular pathway involved in myocardial damage in HF, distinct from the established BNP pathway.
Background:
AXL is a membrane receptor tyrosine kinase highly expressed in the heart and has a conspicuous role in cardiovascular physiology. The role of AXL in heart failure (HF) has not been previously addressed.
Methods And Results:
AXL protein was enhanced 6-fold in myocardial biopsies of end-stage HF patients undergoing heart transplantation compared to controls from heart donors (P<0.0001). Next, we performed a transversal study of patients with chronic HF (n=192) and a group of controls with no HF (n=67). sAXL and BNP circulating levels were quantified and clinical and demographic data were collected. sAXL levels in serum were higher in HF (86.3 ± 2.0 ng/mL) than in controls (67.8 ± 2.0 ng/mL; P<0.0001). Also, sAXL correlated with several parameters associated with worse prognosis in HF. Linear regression analysis indicated that serum creatinine, systolic blood pressure and atrial fibrillation, but not BNP levels, were predictive of sAXL levels. Cox regression analysis indicated that high sAXL values at enrollment time were related to the major HF events (all-cause mortality, heart transplantation and HF hospitalizations) at one year follow-up (P<0.001), adding predictive value to high BNP levels.
Conclusions:
Myocardial expression and serum concentration of AXL is elevated in HF patients compared to controls. Furthermore, peripheral sAXL correlates with parameters associated with the progression of HF and with HF events at short term follow-up. All together these results suggest that sAXL could belong to a new molecular pathway involved in myocardial damage in HF, independent from BNP.
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