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. Author manuscript; available in PMC: 2022 Jan 21.
Published in final edited form as: Thromb Res. 2020 Mar 6;189:77–87. doi: 10.1016/j.thromres.2020.03.003

Table 6:

Treatment Options

Options: Mechanism:
Dysbiosis Prebiotics, probiotics Ingestion of live organisms or supplements to induce growth of certain commensal anaerobes
Antibiotics Depletion of pathogenic microbiota leading to overgrowth of healthy gut flora
Fecal microbial transplant Transplantation of donor fecal samples
LPS C11C1 Monoclonal antibody that blocks LPS binding site
CD14 antibodies Lead to TLR4 internalization and decrease LPS response
Statins Lead to increase expression of LDL-R and increase clearance of LPS
PCSK9 Inhibit degradation of LDL-R leading to increase LPS clearance
IL-1B inhibitors Block downstream TLR4 pathway leading to decrease in CVD
TMAO FMO inhibitors Block conversion of TMA into TMAO
DMB Inhibit microbial TMA lyases to inhibit production of TMA
CutC/D Target microbial proteins

C11C1, HMW Kininogen antibody; LPS, lipopolysaccharides; PCSK9, proprotein convertase subtilisin/ kexin type 9; LDL-R, low density lipoprotein receptor; IL, interleukin; TLR4,toll-like receptor 4; CVD, cardiovascular disease; FMO, Flavin monooxygenases; DMB, 3,3-dimethyl-1-butanol;