Therefore, GSNOR emerges as a critical target for mitigating nitrosative stress during myocardial hypertrophy, which is consistent with the research data that revealed that nitrosative stress in HFpEF was partly due to the impaired activity of GSNOR [70], as well as the reduced levels of GSNOR protein in myocardial samples from patients with hypertrophic cardiomyopathy [71]. This evidence concerns the gene ADH5 and cardiac hypertrophy.