ReviewInternational journal of molecular sciences2018
Potential Role of Humoral IL-6 Cytokine in Mediating Pro-Inflammatory Endothelial Cell Response in Amyotrophic Lateral Sclerosis.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 41 citations in OpenAlex.
- Role of aging‑related cytokines in neurodegenerative disease (Review).International journal of molecular medicine · 2026Review
- The role of adiponectin and cytokines in Amyotrophic lateral sclerosis: assessment of disease progression and survival status.Scientific reports · 2026Article
- A Putative Role for the BCL2 Family of Proteins in the Pathophysiology of ALS.CNS & neurological disorders drug targets · 2026Article
- Elevated peripheral inflammation is associated with choroid plexus enlargement in independent sporadic amyotrophic lateral sclerosis cohorts.Fluids and barriers of the CNS · 2024Article
- The Current Landscape of Hypotheses Describing the Contribution of CD4+ Heterogeneous Populations to ALS.Current issues in molecular biology · 2024Article
- Cellular and molecular mechanisms of the blood-brain barrier dysfunction in neurodegenerative diseases.Fluids and barriers of the CNS · 2024Review
- Genetic Susceptibility in Endothelial Injury Syndromes after Hematopoietic Cell Transplantation and Other Cellular Therapies: Climbing a Steep Hill.Current issues in molecular biology · 2024Review
- The Role of IL-6 in Neurodegenerative Disorders.Neurochemical research · 2024Review
- Association between genetically proxied lipid-lowering drug targets, lipid traits, and amyotrophic lateral sclerosis: a mendelian randomization study.Acta neurologica Belgica · 2024Article
- Article
- The Molecular Link Between TDP-43, Endogenous Retroviruses and Inflammatory Neurodegeneration in Amyotrophic Lateral Sclerosis: a Potential Target for Triumeq, an Antiretroviral Therapy.Molecular neurobiology · 2023Review
- Exploring Relevant Time Windows in the Association Between PM2.5 Exposure and Amyotrophic Lateral Sclerosis: A Case-Control Study in Denmark.American journal of epidemiology · 2023Article
- Autoimmune Neuroinflammatory Diseases: Role of Interleukins.International journal of molecular sciences · 2023Review
- A Brief Overview of Neutrophils in Neurological Diseases.Biomolecules · 2023Review
- Novel pathophysiological insights into CAR-T cell associated neurotoxicity.Frontiers in neurology · 2023Review
- Mechanisms of immune effector cell-associated neurotoxicity syndrome after CAR-T treatment.WIREs mechanisms of disease · 2022Review
- Targeting the Crosstalk of Immune Response and Vascular Smooth Muscle Cells Phenotype Switch for Arteriovenous Fistula Maturation.International journal of molecular sciences · 2022Article
- Functional Impairment of Endothelial Colony Forming Cells (ECFC) in Patients with Severe Atherosclerotic Cardiovascular Disease (ASCVD).International journal of molecular sciences · 2022Article
- Serum biomarkers of neuroinflammation and blood-brain barrier leakage in amyotrophic lateral sclerosis.BMC neurology · 2022Article
- Neuroprotective effects of violacein in a model of inherited amyotrophic lateral sclerosis.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a multifactorial disease with limited therapeutic options. Numerous intrinsic and extrinsic factors are involved in ALS motor neuron degeneration. One possible effector accelerating motor neuron death in ALS is damage to the blood-Central Nervous System barrier (B-CNS-B), mainly due to endothelial cell (EC) degeneration. Although mechanisms of EC damage in ALS are still unknown, vascular impairment may be initiated by various humoral inflammatory factors and other mediators. Systemic IL-6-mediated inflammation is a possible early extrinsic effector leading to the EC death causing central nervous system (CNS) barrier damage. In this review, we discuss the potential role of humoral factors in triggering EC alterations in ALS. A specific focus was on humoral IL-6 cytokine mediating EC inflammation via the trans-signaling pathway. Our preliminary in vitro studies demonstrated a proof of principle that short term exposure of human bone marrow endothelial cells to plasma from ALS patient leads to cell morphological changes, significantly upregulated IL-6R immunoexpression, and pro-inflammatory cell response. Our in-depth understanding of specific molecular mechanisms of this humoral cytokine in EC degeneration may facilitate an endothelial-IL-6-targeting therapy for restoring cell homeostasis and eventually reestablishing B-CNS-B integrity in ALS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.