This discrepancy may be due to the following reasons: in HF patients, the progression of myocardial fibrosis leads to increased local enrichment of HTRA1 in myocardial tissues rather than its release into the bloodstream, resulting in relatively lower plasma levels; HTRA1 may be locally consumed during the myocardial fibrosis process and not sufficiently released into the circulation; or endothelial dysfunction associated with HF may affect the expression and release of HTRA1, with chronic oxidative stress leading to its degradation in the circulatory system. The gene discussed is HTRA1; the disease is endothelial dysfunction.