CO2

CO2gene

CO2 mitochondrial dysfunction elevates ROS production, promoting oxidative lipid modification and systemic inflammation in obesity-associated CAD.

Pathway placement

Cascade stepLipid retention & oxidation

Confidencemedium

RationaleMitochondrial oxidative stress amplifies lipid oxidation and systemic inflammation; obesity association suggests metabolic link to CAD.

Also acts inVascular inflammation

Druggability

Not assessed (no mapped human gene target).

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)-57.2

Confounder panel (Type-II drivers)

1sepsis / systemic inflammationmag 2

2anemia / acute blood lossn/a

3hypovolemia / dehydrationmag 2

4tachyarrhythmiamag 2

5hypoxemia / respiratory failuremag 3

6hypertensive emergencymag 2

7high-demand / peri-operative stressmag 2

Coverage: 6/7 confounders with evidence

Tier: deep-scored (abstract-extracted) · 9 supporting references. See the discrimination table for all markers.

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

Specimen

Whole blood — gene is not a circulating analyte; measure protein product or genotype

Collection tube

K2-EDTA whole blood (lavender-top)

Method / principle

SNP genotyping / sequencing; or immunoassay of encoded protein

Reagent / substrate

Allele-specific primers/probes (TaqMan) or NGS panel; or antibody for protein

Platform

qPCR / NGS / array

Turnaround · availability

Send-out · Genotyping widely available; protein assay variable