What does this research mean for the field?

The PTRF-related TLR4/MyD88-JNK signaling pathway mediates the exacerbation of myocardial ischemia/reperfusion injury caused by concurrent rheumatoid arthritis and a high-fat diet. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This study aims to investigate the mechanisms of coronary heart disease exacerbated by rheumatoid arthritis under the influence of a high-fat diet.

May 24, 2026BiomoleculesOpen Access

Compound Augmentation of Myocardial Injury in a Rat Model of Coronary Heart Disease Induced by Ischemia/Reperfusion, Rheumatoid Arthritis, and High-Fat Diet: A Molecular Mechanistic Study

Q: What is the clinical evidence from this study?

Population: Coronary heart disease associated with rheumatoid arthritis (n=64). Intervention: AAV-mediated knockdown of PTRF vs. Control, I/R alone, HFD alone, CIA alone, and combinations. Primary outcome: Myocardial injury (cardiac injury markers, infarct area, cardiomyocyte apoptosis).

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Key result

AAV-mediated PTRF knockdown attenuates exacerbated myocardial injury in ischemia/reperfusion rats with high-fat diet and arthritis.

n=64

Why the study?

Coronary heart disease associated with rheumatoid arthritis is a primary driver of mortality in rheumatoid arthritis patients, but its pathogenesis under high-fat diet and ischemia/reperfusion requires investigation.

Key Points

This study aims to investigate the mechanisms of coronary heart disease exacerbated by rheumatoid arthritis under the influence of a high-fat diet.
Established a rat model with ischemia/reperfusion, rheumatoid arthritis, and high-fat diet.
Utilized X-ray micro-computed tomography for structural analysis.
Performed transcriptome RNA-seq and immunofluorescence to analyze molecular pathways.
Combined HFD and collagen-induced arthritis significantly elevated cardiac injury markers (CK-MB, LDH, CRP, c-TNT).
Histopathological examination revealed severe myocardial inflammation and fibrosis in I/R + CIA + HFD group.
Activation of TLR4/MyD88 signaling pathway was prominent, with enhanced co-localization of PTRF and TLR4 observed.

Structured PICO

Population

64 male Sprague-Dawley rats

Intervention

Combined cardiac ischemia/reperfusion (I/R), high-fat diet (HFD), and collagen-induced arthritis (CIA), with in vivo shRNA-mediated knockdown of polymerase I and transcription release factor (PTRF)

Comparator

Control, I/R alone, HFD alone, CIA alone, I/R + CIA, HFD + CIA, and I/R + HFD groups

Outcome

Cardiac injury markers (CK-MB, LDH, CRP, c-TNT), infarct area, cardiomyocyte apoptosis, and TLR4/MyD88 signaling pathway activationsurrogate

The PTRF-related TLR4/MyD88-JNK signaling pathway regulates myocardial injury exacerbated by combined high-fat diet and rheumatoid arthritis in a rat model of ischemia/reperfusion.

Discussion

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Implication

PTRF knockdown may modulate diet- and arthritis-worsened myocardial injury in rats; leaves open translation to patients with rheumatoid arthritis and coronary disease.

Cite This Study

Xu et al. (2026) studied Coronary heart disease associated with rheumatoid arthritis (n=64). AAV-mediated knockdown of PTRF vs. Control, I/R alone, HFD alone, CIA alone, and combinations was evaluated on Myocardial injury (cardiac injury markers, infarct area, cardiomyocyte apoptosis). AAV-mediated knockdown of PTRF attenuated the exacerbation of myocardial injury induced by high-fat diet and collagen-induced arthritis in ischemia/reperfusion rats.

synapsesocial.com/papers/6a12962948a0ea1665672bc2 https://doi.org/10.3390/biom16050753

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Implication

PTRF knockdown may modulate diet- and arthritis-worsened myocardial injury in rats; leaves open translation to patients with rheumatoid arthritis and coronary disease.

Compound Augmentation of Myocardial Injury in a Rat Model of Coronary Heart Disease Induced by Ischemia/Reperfusion, Rheumatoid Arthritis, and High-Fat Diet: A Molecular Mechanistic Study

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Compound Augmentation of Myocardial Injury in a Rat Model of Coronary Heart Disease Induced by Ischemia/Reperfusion, Rheumatoid Arthritis, and High-Fat Diet: A Molecular Mechanistic Study

Key Points

Structured PICO

Discussion

Implication

Cite This Study

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