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Trigeminal neuropathic pain (TNP) is a major concern in both dentistry and medicine. The progression from normal to chronic TNP through activation of the insular cortex (IC) is thought to involve several neuroplastic changes in multiple brain regions, resulting in distorted pain perception and associated comorbidities. While the functional changes in the insula are recognized contributors to TNP, the intricate mechanisms underlying the involvement of the insula in TNP processing remain subjects of ongoing investigation. Here, we have overviewed the most recent advancements regarding the functional role of IC in regulating TNP alongside insights into the IC's connectivity with other brain regions implicated in trigeminal pain pathways. In addition, the review examines diverse modulation strategies that target the different parts of the IC, thereby suggesting novel diagnostic and therapeutic management of chronic TNP in the future.
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http://dx.doi.org/10.1186/s10194-024-01784-5 | DOI Listing |
ESC Heart Fail
September 2025
Department of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Heart failure (HF) is a multifactorial and pathophysiological complex syndrome, involving not only neurohormonal activation but also oxidative stress, chronic low-grade inflammation, and metabolic derangements. Central to the cellular defence against oxidative damage is nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor that orchestrates antioxidant and cytoprotective responses. Preclinical in vitro and in vivo studies reveal that Nrf2 signalling is consistently impaired in HF, contributing to the progression of myocardial dysfunction.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
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Achucarro Basque Center for Neuroscience, Leioa, Spain.
Adenosine A receptors (AARs) have shown promising therapeutic properties despite their controversial role in modulating stroke outcome. However, the temporal evolution of cerebral AARs density after cerebral ischemia and its subsequent neuroinflammatory response have been scarcely explored. In this study, the expression of AARs after transient middle cerebral artery occlusion (MCAO) was evaluated in rats by positron emission tomography (PET) with [C]SCH442416 and immunohistochemistry (IHC).
View Article and Find Full Text PDFNeuropsychol Dev Cogn B Aging Neuropsychol Cogn
September 2025
Department of Public Health, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Cognitive function is a critical health indicator of older adults in later life. However, previous research has paid less attention to the impact of pre-retirement work-related characteristics on cognitive functions, especially in Asia. Thus, this study aims to examine the relationship between work-related factors and cognitive functions of the retired population, using Taiwan as an example.
View Article and Find Full Text PDFJ Pathol Transl Med
September 2025
Department of Otorhinolaryngology Head and Neck Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, China.
Background: C-C motif chemokine ligand 3 (CCL3) is a crucial chemokine that plays a fundamental role in the immune microenvironment and is closely linked to the development of various cancers. Despite its importance, there is limited research regarding the expression and function of CCL3 in nasopharyngeal carcinoma (NPC). Therefore, this study seeks to examine the expression of CCL3 and assess its clinical significance in NPC using bioinformatics analysis and experiments.
View Article and Find Full Text PDFMacrophage Migration Inhibitory Factor (MIF) is a pleiotropic cytokine that acts as a central regulator of inflammation and immune responses across diverse organ systems. Functioning upstream in immune activation cascades, MIF influences macrophage polarization, T and B cell differentiation, and cytokine expression through CD74, CXCR2/4/7, and downstream signaling via NF-κB, ERK1/2, and PI3K/AKT pathways. This review provides a comprehensive analysis of MIF's mechanistic functions under both physiological and pathological conditions, highlighting its dual role as a protective mediator during acute stress and as a pro-inflammatory amplifier in chronic disease.
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