ArticleBiology direct2025
Macrophage Notch1 drives septic cardiac dysfunction by impairing mitophagy and promoting NLRP3 activation.
Article in Biology direct, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Mitophagy in pathogenesis and therapeutic implications for infection.Experimental & molecular medicine · 2026Review
- Suppression of Nr1d1/Bnip3-dependent mitophagy by notch signaling aggravates inflammatory response in RSV-infected mice lungs.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Septic Cardiomyopathy: Age-Dependent Physiology and Hemodynamic Aspects-A Narrative Review.Children (Basel, Switzerland) · 2026Review
- Multi-omics analysis identifies NFIL3 as a hypoxia-associated immune regulator in septic cardiomyopathy.Frontiers in immunology · 2026Article
- The central role of mitochondrial pathology in sepsis-induced cardiomyopathy: from molecular mechanisms to clinical translation.Frontiers in cardiovascular medicine · 2026Review
- Mitochondrial dysfunction in sepsis-induced immunoparalysis: from immune-cell metabolic reprogramming to clinical biomarkers.Frontiers in immunology · 2026Review
- Mitochondrial regulation of lactylation in sepsis-induced cardiomyopathy.Critical care (London, England) · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
backgroundSepsis is a life-threatening condition with limited therapeutic options, characterized as excessive systemic inflammation and multiple organ failure. Macrophages play critical roles in sepsis pathogenesis. Although numerous studies support the critical role of Notch signaling in most inflammatory diseases, the function of Notch1 signaling in macrophages activation and its underlying molecular mechanism during sepsis has not been fully elucidated.
methodsWe evaluated Notch1 expression in a lipopolysaccharide (LPS)-induced model of septic cardiac dysfunction. Using macrophage-specific Notch1 knockout mice (NOTCH1
resultsIntraperitoneal injection of LPS markedly impaired cardiac function, increased macrophage infiltration, and elevated Notch1 expression compared with PBS-treated controls. Notch1 expression was inversely correlated with cardiac performance in LPS-treated mice. Notably, macrophage-specific deletion of Notch1 significantly improved cardiac function, whereas NICD1 overexpression worsened LPS-induced cardiac injury. NOTCH1
conclusionOur study uncovers a novel role for Notch1 in exacerbating LPS-induced septic cardiac dysfunction by suppressing mitophagy in macrophages. These findings suggest that targeting Notch1 may offer a promising therapeutic strategy to mitigate sepsis-induced inflammation by restoring proper mitophagy.
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Registered trials
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