Succinate dehydrogenase

SDHAprotein

Succinate dehydrogenase impairment elevates succinate levels, coupling mitochondrial dysfunction to pro-inflammatory innate immune activation in atherosclerotic lesions.

Pathway placement

Cascade stepPlaque inflammation

Confidencemedium

RationaleSDH dysfunction promotes succinate accumulation triggering inflammatory signaling in macrophages.

Druggability

DruggableYes

Known drugs / candidates0

Small-molecule tractableYes

Antibody tractableYes

EnsemblENSG00000073578

Type I vs Type II discrimination

ScoresType-II-associated

R — rupture / Type-I

C — confounder / Type-II

A — assay feasibility

E — evidence strength

T1DI (composite)

Specificity differential (R−C)-55.6

Confounder panel (Type-II drivers)

1sepsis / systemic inflammationmag 2

2anemia / acute blood lossn/a

3hypovolemia / dehydrationmag 2

4tachyarrhythmian/a

5hypoxemia / respiratory failuremag 1

6hypertensive emergencyn/a

7high-demand / peri-operative stressn/a

Coverage: 3/7 confounders with evidence

Tier: deep-scored (abstract-extracted) · 15 supporting references. See the discrimination table for all markers.

Assay & specimen

Class-level default (no specific cleared assay)— generic method inferred from analyte class; confirm against a specific product insert before use.

Specimen

Serum or plasma

Collection tube

Serum separator (gold/red-top, SST) · K2/K3-EDTA (lavender-top)

Method / principle

Sandwich immunoassay (ELISA) — research-grade unless a cleared assay exists

Reagent / substrate

Matched anti-target antibody pair (capture + labeled detection)

Platform

ELISA microplate or multiplex (Luminex/MSD)

Turnaround · availability

Send-out / research · Research-grade (no universal clinical assay)

Literature evidence(1)

Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.
Nature · 2014 · PMID 25383517 · doi