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Войти в исследования Cardiovascular endocrinology & metabolism · 2026
Proteomics analysis of empagliflozin in patients without diabetes or overt heart failure from empagliflozin and cardiac remodeling in people without diabetes CardioLink-7 randomized clinical trial.
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Chen Wei-Siang, Yang Ning-I, Verma Subodh, Liu Min-Hui, Chien Kun-Yi, Chen Chia-Wei, Quan Adrian, Teoh Hwee, Yan Andrew T, Connelly Kim A, Juan Yu-Hsiang, Chang Ching-Wen, Mazer C David, Wang Chao-Hung
Аннотация
BACKGROUND: Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce cardiovascular and cardiorenal events in people across the spectrum of heart failure. Using proteomics analysis, this study investigated the potential benefits of SGLT2 inhibitors in primary prevention at a protein level in patients without diabetes or heart failure.
METHODS: This is a sub-study of the EMPA-HEART 2 CardioLink-7 trial, which randomized people without diabetes or clinically overt heart failure but with risk factors for adverse cardiac remodeling to empagliflozin (10 mg/day) or placebo for 6 months. Blood samples were collected during the randomization visit and at the 6-month follow-up visit for proteomics analysis. Our investigation involved two phases of approach: discovery and verification.
RESULTS: Samples from individuals assigned to empagliflozin (n = 21) and placebo (n = 22) (median baseline N-terminal pro-B-type natriuretic peptide levels: 33.9 and 78.4 pg/ml, respectively) were analyzed. In the discovery phase, 28 of 1622 proteins fulfilled our threshold for being differentially expressed at 6 months. Ten proteins were verified, including calmodulin-like protein 5, desmoplakin, hornerin, peroxiredoxin-2, macrophage colony-stimulating factor 1 receptor, endosialin, high-temperature requirement serine protease A1, immunoglobulin epsilon heavy chain, proteasome subunit beta type-5, and cerebellin-4. Compared to the placebo group, the expression of these proteins from baseline to 6 months was all significantly decreased in the empagliflozin group. Their functions involved ion channel signaling, fibrosis, oxidative stress, inflammation, apoptosis, immune response, proteolysis, and neuromodulation.
CONCLUSION: Empagliflozin modified multiple biologically relevant pathways in the nondiabetes and non-heart failure setting. These findings should be considered hypothesis-generating and warrant validation in larger, adequately powered studies.
METHODS: This is a sub-study of the EMPA-HEART 2 CardioLink-7 trial, which randomized people without diabetes or clinically overt heart failure but with risk factors for adverse cardiac remodeling to empagliflozin (10 mg/day) or placebo for 6 months. Blood samples were collected during the randomization visit and at the 6-month follow-up visit for proteomics analysis. Our investigation involved two phases of approach: discovery and verification.
RESULTS: Samples from individuals assigned to empagliflozin (n = 21) and placebo (n = 22) (median baseline N-terminal pro-B-type natriuretic peptide levels: 33.9 and 78.4 pg/ml, respectively) were analyzed. In the discovery phase, 28 of 1622 proteins fulfilled our threshold for being differentially expressed at 6 months. Ten proteins were verified, including calmodulin-like protein 5, desmoplakin, hornerin, peroxiredoxin-2, macrophage colony-stimulating factor 1 receptor, endosialin, high-temperature requirement serine protease A1, immunoglobulin epsilon heavy chain, proteasome subunit beta type-5, and cerebellin-4. Compared to the placebo group, the expression of these proteins from baseline to 6 months was all significantly decreased in the empagliflozin group. Their functions involved ion channel signaling, fibrosis, oxidative stress, inflammation, apoptosis, immune response, proteolysis, and neuromodulation.
CONCLUSION: Empagliflozin modified multiple biologically relevant pathways in the nondiabetes and non-heart failure setting. These findings should be considered hypothesis-generating and warrant validation in larger, adequately powered studies.