Key result
PBMC profiling in cardiogenic shock reveals upregulated oxidative-stress and matrix-remodeling genes compared to controls.
Why the study?
Cardiogenic shock remains highly lethal with profound immune-inflammatory activation, but molecular signatures in circulating cells are poorly defined.
What are the gene-expression signatures in PBMCs of patients with cardiogenic shock compared to healthy controls, and do they correlate with clinical severity?
Case-Control (n=24)
What are the gene-expression signatures in PBMCs of patients with cardiogenic shock compared to healthy controls, and do they correlate with clinical severity?
PBMC transcriptomics in cardiogenic shock reveals robust activation of oxidative-stress, matrix-remodeling, and cell-death pathways that correlate with clinical severity.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for PBMC biomarkers in cardiogenic shock; larger prospective studies required before clinical translation.
Background Cardiogenic shock (CS) remains highly lethal and is driven by hemodynamic collapse with profound immune-inflammatory activation. Molecular signatures in circulating cells are poorly defined. Objectives To characterize gene-expression signatures in peripheral blood mononuclear cells (PBMCs) from patients with cardiogenic shock and identify pathways and candidate biomarkers associated with clinical severity. Methods We studied 12 CS patients (SCAI C–E; ischemic n=7, non-ischemic n=5) and 12 sex/age/BMI-matched healthy controls. Peripheral blood mononuclear cells (PBMCs) were isolated within 24 h of presentation. An exploratory PrimePCR array profiled 96 targets in 5 AMI-CS vs 5 controls. Differentially expressed genes were then validated by RT-qPCR in the full cohort (12 CS vs 12 controls). Relative expression was calculated by 2^-ΔΔCt. Clinical–molecular correlations used Pearson coefficients. Results In the exploratory set, CS showed up-regulation of MMP9, CHI3L1, SOD2, and PKM2 (all p=0.031–0.016) and down-regulation of TBX21 and CD28 (both p=0.031). In the validation cohort, expression of MMP9, TIMP1, SOD2, CAT, GPX1, NOX2, and CASP3 was higher in CS than controls (p≤0.022; MMP9/TIMP1/SOD2 p<1×10^-6). Molecular signals related to clinical severity: MMP9 correlated with SCAI class and lactate (r=0.71 and 0.78), SOD2 with SCAI and CRP (r=0.77 and 0.91) and with CICU death (r=0.66), NOX2 with troponin and CRP (r=0.82 and 0.92), and TIMP1 with troponin and CRP (r=0.79 and 0.80). Conclusions PBMC transcriptomics in CS highlights robust activation of oxidative-stress (SOD2/CAT/GPX1/NOX2), matrix-remodeling (MMP9/TIMP1), and cell-death/survival (CASP3/PKM2) pathways, with relative down-modulation of Th1/adaptive immunity (TBX21/CD28). These hypothesis-generating data nominate readily accessible candidate biomarkers linked to clinical severity and suggest testable, disease-modifying pathways for validation and proteomic integration in larger cohorts.validation analysis correlation analysis
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Filomia et al. (2026) conducted a case-control in Cardiogenic shock (n=24). PBMC gene expression profiling vs. Healthy controls was evaluated on Differential gene expression in peripheral blood mononuclear cells (p=<1x10^-6). PBMC gene expression profiling in cardiogenic shock revealed significant upregulation of oxidative-stress and matrix-remodeling genes like MMP9, TIMP1, and SOD2 compared to controls (p<1x10^-6).
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