Parker, Mao, Caudell, Seals, Wang, Green, McClung, Maxwell, Roddey, Shakeriastani, Wu, Lu, Kim, Fert-Bober, Du, Bhat, Sundararaman, Ayres, Pandey, . . . Herrington (2026). Molecular mechanism leading to human coronary atherosclerosis assessed by proteomic analysis and RNA sequences.. European heart journal.
Parker, Mao, Caudell, Seals, Wang, Green, et al. Molecular mechanism leading to human coronary atherosclerosis assessed by proteomic analysis and RNA sequences.. European heart journal. 2026; PMID: 42119148
Parker, Mao, Caudell, et al. Molecular mechanism leading to human coronary atherosclerosis assessed by proteomic analysis and RNA sequences.[J]. European heart journal. 2026.
@article{parker2026,
author = {Parker and Mao and Caudell and Seals and Wang and Green and McClung and Maxwell and Roddey and Shakeriastani and Wu and Lu and Kim and Fert-Bober and Du and Bhat and Sundararaman and Ayres and Pandey and Bhardwaj and Karere and Troxclair and Jackson and Love and Vander Heide and Hixson and Van Eyk and Wang and Herrington},
title = {Molecular mechanism leading to human coronary atherosclerosis assessed by proteomic analysis and RNA sequences.},
journal = {European heart journal},
year = {2026},
note = {PMID: 42119148},
}
TY - JOUR AU - Parker AU - Mao AU - Caudell AU - Seals AU - Wang AU - Green AU - McClung AU - Maxwell AU - Roddey AU - Shakeriastani AU - Wu AU - Lu AU - Kim AU - Fert-Bober AU - Du AU - Bhat AU - Sundararaman AU - Ayres AU - Pandey AU - Bhardwaj AU - Karere AU - Troxclair AU - Jackson AU - Love AU - Vander Heide AU - Hixson AU - Van Eyk AU - Wang AU - Herrington TI - Molecular mechanism leading to human coronary atherosclerosis assessed by proteomic analysis and RNA sequences. T2 - European heart journal PY - 2026 AN - PMID:42119148 ER -
Atherosclerosis results from cellular and extracellular changes in the arterial wall, preceded by molecular shifts that initiate disease and drive tissue conversion, yet these changes are not yet fully described. More data are needed concerning these early changes in the coronary artery molecular landscape that signify the initiation of atherosclerosis and the subsequent tissue pheno-conversion to atherosclerotic plaque. This report summarizes results from a large biorepository of human coronary artery tissue, applying state-of-the-art omics technology, advanced data analytic methods, and an arterial organoid model system to predict molecular dynamics and identify potential regulatory mechanisms that could interrupt molecular changes that contribute to the earliest stages of disease pathogenesis. The long-term goal of this effort is to identify and develop new therapies to further mitigate the persistently high burden of clinical coronary disease.