bims-migras 2026-07-26 papers

Issue of 2026–07–26
two papers selected by
Cliff Dominy

J Extracell Vesicles. 2026 Jul;15(7): e70338

S100A9 Aggravates Cardiac Fibrosis by TLR4/PGC-1α Mediated Macrophage-Myofibroblast Crosstalk.

Yiting Zhao, Yaqin Zhang, Qiang Yuan, XiaoFeng Fang, Jianlong Sheng, Yuhang Deng, Shichun Shen.

Fibrosis is a critical component of ventricular remodelling after myocardial ischemia, and the activation and expansion of cardiac fibroblasts represent key drivers of this process. Our previous work identified S100A9-dependent macrophage-to-myofibroblast transition (MMT) as a newly recognized source of myofibroblasts in the post-MIR heart. However, the mechanisms by which S100A9 regulates MMT remain incompletely understood. Here, using multiple genetically engineered mouse models, MIR and MI model, and in vitro multicellular co-culture systems, we investigated the role of S100A9 in regulating fibroblast-derived migrasome release during MMT. We found that macrophage-derived S100A9 promotes mitochondrial dysfunction and migrasome release in cardiac fibroblasts through TLR4/PGC1α signalling following MIR. These fibroblast-derived migrasomes, in turn, activate integrin/Src signalling in macrophages, triggering MMT and accelerating cardiac fibrosis. Importantly, we delineate how macrophage-derived S100A9 orchestrates crosstalk between fibroblasts and immune cells and identify migrasome-mediated activation of MMT as a previously unrecognized mechanism driving post-MIR fibrotic remodelling. Our findings suggest that targeting S100A9-induced migrasome release and downstream MMT signalling may represent a promising therapeutic strategy to mitigate pathological cardiac fibrosis.

Keywords: PGC1α; S100A9; macrophage‐to‐myofibroblast transition; migrasome; mitochondria

DOI: https://doi.org/10.1002/jev2.70338

Front Cell Infect Microbiol. 2026 ;16 1864492

Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.

Yu Ruoting, Lei Jinlin, Liu Yuhao, Fang Zemin, Gao Wei.

Neutrophils (NE) and macrophages (Mø) are canonical cellular components of the innate immune defense and are involved throughout the course of acute lung injury (ALI). The crosstalk between these two cell types is pivotal for elucidating the complex mechanisms underlying inflammation. This review focuses on the bidirectional interactions between NE and Mø mediated by cytokines and phagocytosis. In addition, emerging concepts, including exosomes and migrasomes, are discussed to further delineate the role of NE in this crosstalk network. Certain pro-inflammatory cytokines amplify inflammation through cascade effects, ultimately leading to a cytokine storm. Pro-inflammatory and anti-inflammatory processes are dynamically coordinated and diverge at key regulatory nodes, forming multiple positive and negative feedback loops that collectively establish the inflammatory network model of ALI. The terminal outcome of this network is cell death, encompassing apoptosis, necroptosis, pyroptosis, and PANoptosis. By integrating the crosstalk network with cell death pathways, a more comprehensive regulatory framework is constructed, enabling an in-depth exploration of the molecular mechanisms underlying ALI.

Keywords: PANoptosis; acute lung injury; cytokines; macrophages; neutrophils

DOI: https://doi.org/10.3389/fcimb.2026.1864492