Key result
Mdivi-1 reduces OxLDL-induced glycolysis, CXCL8 expression, and foam cell formation in human monocytes.
Why the study?
Do Mdivi-1 and S1QEL attenuate oxidized LDL-induced glycolytic reprogramming, inflammatory cytokine expression, and foam cell formation in primary human monocytes?
Do Mdivi-1 and S1QEL attenuate oxidized LDL-induced glycolytic reprogramming, inflammatory cytokine expression, and foam cell formation in primary human monocytes?
Answers are grounded in this paper and cite their sources.
Inhibiting mitochondrial fission with Mdivi-1 or complex I mitochondrial ROS with S1QEL suppresses OxLDL-induced glycolytic reprogramming, inflammatory signaling, and foam cell formation in human monocytes, identifying potential cellular targets to slow atherogenesis.
Atherosclerosis, a major contributor to cardiovascular disease, involves lipid accumulation and inflammatory processes in arterial walls, with oxidized low-density lipoprotein (OxLDL) playing a central role. OxLDL is increased during aging and stimulates monocyte transformation into foam cells and induces metabolic reprogramming and pro-inflammatory responses, accelerating atherosclerosis progression and contributing to other age-related diseases. This study investigated the effects of Mdivi-1, a mitochondrial fission inhibitor, and S1QEL, a selective complex I-associated reactive oxygen species (ROS) inhibitor, on OxLDL-induced responses in monocytes. Healthy monocytes isolated from participants were treated with OxLDL, with or without Mdivi-1 or S1QEL, and assessed for metabolic shifts, inflammatory cytokine expression, foam cell formation, and ROS production. OxLDL treatment elevated glycolytic activity (ECAR) and expression of pro-inflammatory cytokines IL1B and CXCL8, promoting foam cell formation and mitochondrial ROS (mtROS) production. Mdivi-1 and S1QEL effectively reduced OxLDL-induced glycolytic reprogramming, inflammatory cytokine levels, and foam cell formation while limiting mtROS. These findings suggest that both Mdivi-1 and S1QEL modulate key monocyte responses to OxLDL, providing insights into potential therapeutic approaches for age-related diseases.
No takes yet. Share an insight, caveat, or question.
Mosalmanzadeh et al. (2026) studied Atherosclerosis (ex vivo human monocytes exposed to oxidized LDL). Mdivi-1 or S1QEL co-treatment with oxidized LDL (OxLDL) vs. Oxidized LDL (OxLDL 2.5 mg/mL or DiI-OxLDL 1 mg/mL) alone and media-only control was evaluated on Extracellular acidification rate (ECAR) area under the curve (glycolytic activity), pro-inflammatory cytokine gene expression (CXCL8, IL1B), and foam cell formation (p=0.027). Mdivi-1 significantly reduced OxLDL-induced glycolytic activity (p=0.027), CXCL8 expression (p<0.001), and foam cell formation (p=0.0395) in primary human monocytes.
Synapse has enriched 10 related papers. Consider them for comparative context: