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CO2
Pathway / Lipid retention & oxidation

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 non-Type I discrimination

ScoresNon-Type-I-associated
R — rupture / Type-I
C — non-Type-I
71
A — assay feasibility
52
E — evidence strength
5
T1DI (composite)
1
Specificity differential (R−C)-56.4
Non-Type-I axis panel
Does this marker also move in each non-Type-I setting? mag 0–3; higher means less Type-I-specific. n/a = no evidence retrieved, which is not the same as no change.
2sepsis / systemic inflammationmag 2
2anemia / acute blood lossn/a
2hypovolemia / dehydrationmag 2
2tachyarrhythmiamag 2
2hypoxemia / respiratory failuremag 3
2hypertensive emergencymag 2
2high-demand / peri-operative stressmag 2
3sudden cardiac deathmag 2
4aPCI-related periproceduraln/a
4bstent thrombosisn/a
4cin-stent restenosisn/a
5CABG-relatedn/a
Coverage: 7/12 axes with evidence
Tier: deep-scored (abstract-extracted) · 10 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
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

Literature evidence(1)