ArticleCell death & disease2025
HUMANIN produced by human efferocytic macrophages promotes the resolution of inflammation.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Humanin Attenuates Inflammatory Liver Injury and NF-κB Activation During Systemic HypervirulentPathogens (Basel, Switzerland) · 2026Article
- Repeated Humanin Treatment Attenuates Oxidative Stress, Inflammation, and Apoptosis in Diabetic Cardiac Tissue.Biology · 2026Article
- Inflammation and wound healing: a comprehensive overview of mechanisms, therapeutic strategies, and translational perspectives.Biomarker research · 2026Review
- Mitochondrion-targeted therapies for diabetic wound healing: from mechanism to therapeutic opportunity.Burns & trauma · 2026Review
- Human microglia differentially respond to β-amyloid, tau, and combined Alzheimer's disease pathologies in vivo.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
Elimination of apoptotic neutrophils by macrophages, a process called efferocytosis, is a critical step in the resolution of inflammation. Efferocytosis induces the reprogramming of macrophages towards a pro-resolving phenotype and triggers the secretion of pro-resolving factors. While mouse efferocytic macrophages are well-described, less is known about human efferocytic macrophages. Here, using RNA sequencing analysis of three different types of in vitro-derived human efferocytic macrophages, we observed a common modulation of mitochondrial metabolism-related genes in human M0, M1, and M2a-like macrophages, thus correlating with some previous results obtained in other non-human models. These results led us to identify for the first time some particular genes regulated in humans like PLIN5 and MTLN. We also shed light on a mitochondrial gene (MT-RNR2) coding a secreted factor called HUMANIN. Mainly known for its antioxidant and neuroprotective effects, we found that HUMANIN was also associated with pro-resolving properties in human and mouse models. Indeed, HUMANIN was produced early during the resolution of inflammation in an acute peritonitis mouse model. Preventive HUMANIN administration in this model reduced leukocyte infiltration and pro-inflammatory cytokine secretion. These anti-inflammatory properties were accompanied by the early acquisition of a CD11b
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