SynthesisJournal of perinatal medicine2026
Inflammasome biology in preeclampsia: from Bnip3-mitophagy to Nlrp1-driven placental injury - a systematic review and translational roadmap.
Synthesis in Journal of perinatal medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
31 authors.
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Abstract
introductionAlthough inflammasome activation has been repeatedly linked to preeclampsia, the field has tended to frame this biology around NLRP3 alone, leaving other sensors - particularly NLRP1 - and their mitochondrial upstream signals only partially examined. Recent experimental work hints at a more intricate narrative in which dysregulated BNIP3-mediated mitophagy and escalating mitochondrial ROS form a convergent pathway toward trophoblast injury. Yet no systematic review has stitched these elements together. CONTENT: Following PRISMA 2020 guidance, we synthesized evidence across experimental, observational, and mechanistic studies, mapping how impaired mitochondrial quality control, oxidative stress, and inflammasome signaling intersect within the placenta and maternal vasculature. The retrieved literature was analyzed for methodological transparency and biological coherence, allowing a layered reconstruction of how BNIP3 overexpression, mitophagy failure, and mtROS collectively prime NLRP1 activation. SUMMARY: Across 31 eligible studies, a consistent picture emerged: mitochondrial injury acts less as a by-product and more as a central instigator of the inflammatory cascade that shapes the preeclampsia phenotype. The BNIP3→mtROS→NLRP1 axis appears particularly relevant, even when data are fragmented or derived from heterogeneous models. OUTLOOK: Recognizing this pathway opens conceptual space for a new therapeutic toolkit - one aimed at mitochondrial stabilization, inflammasome modulation, and restoring trophoblast resilience.
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