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This article explores the role of the macrophage YTHDC1/TIGAR/NF-κB axis in pulmonary hypertension and highlights its potential as a therapeutic target to mitigate inflammation-driven vascular remodeling.
Identification of a pathogenic E. coli strain overexpressing HtpG that promotes fibrosis in chronic pancreatitis via macrophage-mediated pathways highlights new microbiota-targeted treatment avenues.
This article reviews recent evidence on how HBV manipulates monocyte-to-macrophage differentiation through metabolic and epigenetic reprogramming, facilitating immunosuppression and chronic infection.
This study reveals distinct sex differences in skeletal muscle inflammation and dysfunction in patients with HFrEF, highlighting divergent immune cell profiles linked to muscle mass and strength variations in men versus women, advancing und
NSUN6 deficiency in pancreatic cancer promotes immune suppression by enhancing immunosuppressive macrophage infiltration via the KDM5A-CCL2 axis, leading to resistance to immune checkpoint blockade; targeting this pathway offers a promising
Spatially distinct macrophage subsets interact with heterogeneous myofibroblast populations in lupus nephritis, driving maladaptive fibrosis and chronic kidney injury. Identifying these fibroinflammatory circuits offers promising targets fo
This study uses single-cell RNA sequencing of bronchoalveolar lavage cells to reveal immune dysregulation in COPD, highlighting profibrotic macrophages and monocytes as key players in airway remodeling and gas exchange impairment.
A 2026 European Heart Journal study identifies macrophage circHIPK2 as a regulator of post-MI inflammation and fibrosis, with macrophage-targeted silencing improving cardiac remodeling in mice and showing translational promise in human myoc
A 2026 European Heart Journal study identifies macrophage circHIPK2 as a regulator of post-MI inflammation and fibrosis, integrating circular RNA biology with macrophage polarization, stress-granule signaling, and emerging immune-targeted R
Researchers using human stem cell models have discovered that macrophages actively amplify the electrical signals of damaged nerves, driving the spontaneous pain characteristic of neuropathy, offering a new target for non-opioid pain relief
A groundbreaking human iPSC-derived co-culture study reveals that macrophages respond to neuronal injury by adopting a pro-algesic state, directly intensifying spontaneous neuronal firing—a key driver of chronic neuropathic pain and a novel
Researchers have discovered that the protein PRMT9 plays a vital role in healing the heart after a myocardial infarction by controlling inflammatory macrophages. By promoting the degradation of the STAT1 protein, PRMT9 reduces tissue damage
