TCA metabolite
Extramitochondrial succinate signaling↓
Also searched as Extramitochondrial succinate signaling.
A metabolite that became a messenger. Succinate accumulation stabilizes hif-1-alpha and drives IL-1-beta in macrophages, and on reperfusion its rapid re-oxidation is a principal source of the injury burst. An intermediate of normal energy metabolism doing damage by being in the wrong place at the wrong concentration.
In depth
Accumulates under ischemia and acts outside the mitochondrion as an inflammatory signal.
What drives it
Mitochondrial energy increases it.
A normal TCA intermediate. Carried by the intermediary-metabolism, micronutrient and redox reviews. doi 10.3390/nu18132141 · PMC9967593
What it drives
It increases Calms body-wide inflammation.
A metabolite that became a messenger - succinate accumulation stabilizes HIF-1-alpha and drives IL-1-beta in macrophages. Carried by the intermediary-metabolism, micronutrient and redox reviews. doi 10.3390/nu18132141 · PMC9967593
It increases Inflammatory alarm.
Via the IL-1-beta arm. Carried by the intermediary-metabolism, micronutrient and redox reviews. doi 10.3390/nu18132141 · PMC9967593
It increases Oxidative stress.
On reperfusion its rapid re-oxidation is a principal source of the injury burst. Carried by the intermediary-metabolism, micronutrient and redox reviews. doi 10.3390/nu18132141 · PMC9967593
It reduces Cardiac output.
The ischemia-reperfusion mechanism. Carried by the intermediary-metabolism, micronutrient and redox reviews. doi 10.3390/nu18132141 · PMC9967593
It increases The Metabolite Veto.
Succinate is the endogenous ligand of the GPR91/SUCNR1 receptor. doi 10.1016/j.celrep.2021.109246
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.