Sterile inflammation in laminopathies

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Sterile inflammation, an immune response triggered in the absence of pathogens, plays a key role in various chronic diseases, including aging-related disorders, cancer, and autoimmune conditions. This process is driven by damage-associated molecular patterns, such as self-DNA in the cytosol, which activate innate immune pathways and contribute to persistent inflammation. Chronic activation of these pathways exacerbates tissue damage and accelerates disease progression. Recent studies have connected sterile inflammation to laminopathies, a group of genetic disorders caused by mutations in the LMNA gene, which encodes nuclear intermediate filament proteins essential for nuclear structure and function. In this review we discuss the molecular mechanisms underlying sterile inflammation in laminopathies, emphasizing self-DNA sensing, inflammatory signaling cascade activation, and their pathological consequences. Additionally, we explore potential therapeutic strategies aimed at modulating inflammation and improving disease outcomes. Understanding these interactions may provide new avenues for targeting inflammation in laminopathies and related conditions.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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