Results 51 to 60 of about 9,881 (141)
The Journal of Physiology, EarlyView.Abstract figure legend Mitochondria are highly dynamic organelles that continuously remodel their architecture through coordinated cycles of fusion and fission. This review examines the four key GTPases that orchestrate mitochondrial dynamics in mammals: MFN1, MFN2, OPA1, and DRP1.
Rémi Chaney +4 more
wiley +1 more source
Engineering Efferocytosis for Bone Regeneration
Macromolecular BioscienceABSTRACTBone is an incredibly robust tissue thanks to its high blood supply, rapid cell turnover, and continuous remodeling. A significant body of research investigates strategies to improve osteogenesis, angiogenesis, and immunomodulation for bone regeneration, facilitated by numerous various therapeutic approaches (e.g.
Jacob Miszuk, Linna Zhong, Hongli Sun
openaire +2 more sources
Aspartame Increases the Risk of Pancreatic Ductal Adenocarcinoma
eFood, Volume 7, Issue 3, June 2026.Aspartame (APM) is a widely used artificial sweetener associated with various health concerns, including potential links to diabetes, cardiovascular diseases, and an increased risk of cancer. A comprehensive approach incorporating data mining, machine learning, network toxicology, molecular docking, molecular dynamics simulations, and clinical sample ...
Jumin Xie +5 more
wiley +1 more source
Protein Science, Volume 35, Issue 6, June 2026.Abstract The leucine‐rich repeat‐containing G protein‐coupled receptor 6 (LGR6) has a potential role in inflammation resolution and different cancer processes. In this study, we employed computational techniques, including molecular docking and molecular dynamics simulations of mammalian membrane‐embeded systems, to understand the activation mechanism ...
Álex Pérez‐Sánchez +3 more
wiley +1 more source
Acalabrutinib in Chronic Lymphocytic Leukemia: Pharmacology and Emerging Clinical Perspectives
European Journal of Haematology, Volume 116, Issue 6, Page 759-770, June 2026.ABSTRACT Acalabrutinib, a second‐generation Bruton's tyrosine kinase inhibitor (BTKi), is characterized by enhanced specificity and selectivity for BTK with minimal off‐target effects, offering a significant evolution in the treatment of chronic lymphocytic leukemia (CLL). Its mechanism of action, a covalent binding to Cys481 within the BTK active site,
Gianluca Gaidano, Romano Danesi
wiley +1 more source
Efferocytosis in the Tumor Microenvironment [PDF]
, 2016 Cell death in response to physiological cues is a feature of many normal tissues, and often occurs due to tissue damage or disease. Regardless of the reason, dying cells require their rapid removal from the tissue in order to maintain homeostasis in the tissue, prevent potential cytotoxic immunity against self-antigens, and to promote wound healing ...
D.B. Vaught, J.C. Stanford, R.S. Cook
openaire +1 more source
Macrophage‐Fibroblast Crosstalk Shapes Wound Repair Signaling In Vitro
The FASEB Journal, Volume 40, Issue 10, 31 May 2026.Intercellular communication between macrophages and fibroblasts is critical for wound healing. Macrophages promoted fibroblast scratch closure through contact‐dependent mechanisms independent of connexins. In contrast, fibroblasts regulated macrophage cytokine secretion via connexin‐43–mediated contact signaling that increased IL10 and paracrine ...
Daniela Enriquez‐Ochoa +12 more
wiley +1 more source
Regulated Cell Death in Idiopathic Pulmonary Fibrosis
The FASEB Journal, Volume 40, Issue 9, 15 May 2026.This graphical abstract illustrates regulated cell death (RCD) across key pulmonary cell types—including alveolar epithelial cells, fibroblasts, macrophages, and endothelial cells—modulated through a dynamic death modulation network within the IPF microenvironment.
Xiaoyue Pan +10 more
wiley +1 more source
Neutrophil efferocytosis in chronic inflammatory gastrointestinal diseases: mechanistic insights and therapeutic potential. [PDF]
Front ImmunolYe SY +6 more
europepmc +1 more source
Impaired Macrophage Efferocytosis: Shared Mechanisms and Therapeutic Implications in Immune-Mediated Inflammatory Diseases. [PDF]
J Inflamm ResHe Z, Chen N, Zhang Y, Du H, Jie L.
europepmc +1 more source