Myocardial injury in systemic lupus erythematosus and lupus nephritis: A silent threat

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  Figure 1:. Immune-mediated mechanisms linking SLE to cardiovascular disease. Impaired clearance of apoptotic material triggers activation of endosomal Toll-like receptors (TLRs) and a type I interferon (IFN)-driven inflammatory response. Innate immune pathways—including NET formation, low-density granulocytes, and macrophage activation—promote endothelial dysfunction, oxidative stress, and vascular inflammation. Type I IFNs further impair endothelial repair and angiogenesis, contributing to a pro-atherogenic environment. Adaptive immune responses, through autoantibody production and pro-inflammatory T-cell activity, amplify vascular injury and immunothrombosis. These interconnected mechanisms ultimately lead to accelerated atherosclerosis, thrombosis, and myocardial inflammation, underlying the increased cardiovascular burden in patients with SLE. Created in BioRender. MOYSIDOU, E. (2026) https://BioRender.com/fcmmtww Abbreviations: Anti-dsDNA, anti double-stranded DNA antibodies; anti-SSA/Ro, anti-Sjögren’s syndrome A antibodies; Bregs, B regulatory cells; EPCs, endothelial progenitor cells; IL, interleukin; IL-R, interleukin receptor; SMPC, smooth muscle progenitor cells; Th1, T-helper 1;…

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  Figure 2:. Predisposing factors and immune mechanisms leading to pericarditis in SLE.

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  Figure 3:. Proposed clinical approach to the assessment of cardiac involvement in patients with SLE and LN.

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  Figure 4:. Lupus myocarditis in SLE: histopathological findings. Myocardial involvement in lupus myocarditis is characteristically patchy and subject to sampling error; a negative EMB therefore does not exclude active disease. Created in BioRender. MOYSIDOU, E. (2026) https://BioRender.com/fcmmtww