Two point mutations in the hepatitis B virus core promoter, A1762T/G1764A and G1896A, track with rougher liver disease, yet clinicians have had little serum-level signal to tell one chronic infection from another. A study in iScience ran 108 treatment-naive chronic hepatitis B patients through multi-omics integration, pairing data-independent acquisition serum proteomics with untargeted metabolomics. One pathway kept surfacing across every comparison: cholesterol metabolism.

Diabetic heart failure remains a leading cause of cardiovascular death, yet the precise lipid species that push the diabetic myocardium toward dysfunction have stayed elusive. A 2026 study in Cardiovascular Diabetology: Endocrinology Reports applied multi-omics integration to human heart tissue, pairing untargeted lipidomics, metabolomics, and quantitative proteomics from the same myocardial samples. The authors uncovered what they call electrostatic lipidopathy, a charge-dep