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Understanding inflammatory pathways in cardiovascular diseases: A step toward targeted anti-inflammatory therapies

Syed Muhammad Essa

Syed Muhammad Essa

Bolan Medical complex hospital QuettaQuetta, Pakistan
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Essa, Syed Muhammad
, 
Abdul Ghaffar

Abdul Ghaffar

Bolan Medical complex hospital QuettaQuetta, Pakistan
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Ghaffar, Abdul
, 
Milica Jovanovic

Milica Jovanovic

University of Tartu, Tartu Ulikool
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Jovanovic, Milica
, 
Abdul Khaliq

Abdul Khaliq

Bolan Medical complex hospital QuettaQuetta, Pakistan
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Khaliq, Abdul
 and 
Muhammad Imran Usmani

Muhammad Imran Usmani

Department of Pediatric and Child Health, The Aga Khan UniversityKarachi,
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Usmani, Muhammad Imran
  
Sep 04, 2025
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Article Category: Review
Published Online: Sep 04, 2025
DOI: https://doi.org/10.2478/rjc-2025-0025
Keywords
© 2024 Syed Muhammad Essa et al., published by Sciendo
This work is licensed under the Creative Commons Attribution 4.0 International License.

Figure 1

Detailed illustration of the NLRP3 inflammasome activation in cardiovascular disease, showing both inactive and active states, activation signals, cardiovascular disease triggers, downstream effects, and therapeutic targets.
Detailed illustration of the NLRP3 inflammasome activation in cardiovascular disease, showing both inactive and active states, activation signals, cardiovascular disease triggers, downstream effects, and therapeutic targets.

Figure 2

Visual representation of the complex inflammatory processes in atherosclerosis, including endothelial dysfunction, monocyte recruitment, foam cell formation, adaptive immune responses, and potential therapeutic interventions.
Visual representation of the complex inflammatory processes in atherosclerosis, including endothelial dysfunction, monocyte recruitment, foam cell formation, adaptive immune responses, and potential therapeutic interventions.

Figure 3

side-by-side comparison of inflammatory mechanisms in heart failure (both HFrEF and HFpEF) and the temporal progression of inflammation following myocardial infarction.
side-by-side comparison of inflammatory mechanisms in heart failure (both HFrEF and HFpEF) and the temporal progression of inflammation following myocardial infarction.

Clinical Trials Summary: CANTOS, COLCOT, and LoDoCo2 with Statistical Results_

Trial Name Target/Intervention Study Population Primary Endpoint Key Findings Statistical Results
CANTOS Canakinumab (IL-lß inhibitor) Post-MI patients with elevated hs-CRP (>2 mg/L) MACE (CV death, MI, stroke) Reduced MACE independent of lipid levels; no LDL-C change; ↑ infection risk HR = 0.85; 95% CI: 0.74-0.98; p = 0.021
COLCOT Low-dose Colchicine (0.5 mg/day) Patients within 30 days post-MI Composite CV death, cardiac arrest, MI, stroke, angina, hospitalization 23% relative risk reduction in the primary endpoint HR = 0.77; 95% CI: 0.61-0.96; p = 0.02
LoDoCo2 Low-dose Colchicine (0.5 mg/day) Stable coronary artery disease patients Composite CV death, MI, stroke, or ischemia-driven revascularization 31% relative risk reduction in the primary endpoint HR = 0.69; 95% CI: 0.57-0.83; p < 0.001
Language:
English
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4 times per year
Journal Subjects:
Medicine, Clinical Medicine, Internal Medicine, Cardiology, Surgery, Cardiac Surgery, Pediatrics and Juvenile Medicine, Paediatric Cardiology
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