NMDAR
proteinNMDAR activation mediates excitotoxic calcium overload and mitochondrial damage in ischemic myocardial injury.
Pathway placement
Cascade stepMyocardial injury (shared endpoint)
Confidencemedium
RationaleN-methyl-D-aspartate receptor; ischemic cardiomyocyte death via excitotoxicity.
Druggability
Not assessed (no mapped human gene target).
Type I vs Type II discrimination
ScoresLow-confidence (proxy)
R — rupture / Type-I37
C — confounder / Type-II81
A — assay feasibility68
E — evidence strength30
T1DI (composite)6
Specificity differential (R−C)-43.8
Confounder panel (Type-II drivers)
No confounder evidence retrieved.
Tier: light (literature co-occurrence proxy — lower confidence). 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)
- A Metabolomics-Based Study on NMDAR-Mediated Mitochondrial Damage through Calcium Overload and ROS Accumulation in Myocardial Infarction.Frontiers in bioscience (Landmark edition) · 2023 · PMID 37525913 · doi