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July 22, 2026MedCommOpen Access

Cardiovascular inflammation drives disease progression, with mitochondrial DAMPs linking metabolic stress to sterile immune activation.

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Review

Key result

Cardiovascular inflammation acts as a determinant of disease initiation and progression, with mitochondrial quality control and DAMPs linking metabolic stress to sterile immune activation.

Authors

JRJiaxiang RongZWZ P WangXLXiaoxiao Lin

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Overview

Leaves open clinical adoption of targeted DAMP modulation in CVD; hypothesis-generating for network-based strategies pending prospective trials.

Key Points

  • This research aims to clarify the role of inflammation and immunity in cardiovascular disease development and progression.
  • Synthesis of evidence on immune landscapes and inflammatory networks in cardiovascular diseases.
  • Focus on specific signaling pathways like TLR–NF‐κB and NLRP3 inflammasomes.
  • Discussion of therapeutic strategies and biomarkers for cardiovascular inflammation.
  • Identified interconnected circuits of immune activation linking metabolic stress to cardiovascular damage.
  • Highlighted the role of mitochondrial DAMPs in initiating sterile immune activation.
  • Proposed a shift from broad anti-inflammatory therapies to targeted network regulation strategies.

PICO

P
Population
Cardiovascular disease

Provides a conceptual basis for moving cardiovascular inflammatory therapy from broad suppression toward more precise network regulation.

Cite This Study

Rong et al. (2026) conducted a review in Cardiovascular disease. Cardiovascular inflammation acts as a determinant of disease initiation and progression, with mitochondrial quality control and DAMPs linking metabolic stress to sterile immune activation.

synapsesocial.com/papers/6a605d4a4163e025518d766ahttps://doi.org/10.1002/mco2.70878
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