ReviewBiomedicines2020
Endoplasmic Reticulum Stress in Macrophages: The Vicious Circle of Lipid Accumulation and Pro-Inflammatory Response.
Review in Biomedicines, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Gender correlation between sleep duration and risk of coronary heart disease: a systematic review and meta-analysis.Frontiers in cardiovascular medicine · 2025Pooled it
- Atherosclerotic Cell Fates: A Single-Cell View of ER Stress.Journal of cardiovascular development and disease · 2026Review
- Nanoplastic Particle Exposure Induces Toxicity and Amplifies Cellular Stress in THP-1 Macrophages: Insights on Molecular Pathways and Circulating Proteome Interaction.Journal of biochemical and molecular toxicology · 2026Article
- Neutrophil-Mediated Inflammatory Response to Zinc Bone Implants: A Single-Cell Transcriptomic Landscape.Advanced healthcare materials · 2026Article
- Loss of Echs1 in neural stem and progenitor cells impairs neurogenesis via ER stress activation and lipid metabolic reprogramming.Nature communications · 2026Article
- PERK Is Dispensable for Smooth Muscle Cell Phenotype Switching in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Macrophage efferocytosis in cardiovascular disease: mechanisms and therapeutic implications.ImmunoHorizons · 2026Review
- Vitamin D Reprograms Non-Coding RNA Networks to Block Zika Virus in Human Macrophages.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Activating transcription factors: Orchestrators of macrophage biology in pathological settings (Review).International journal of molecular medicine · 2026Review
- Dysfunction of lipid metabolism and lysosomal capacity: at the core of microglial aging?Frontiers in aging neuroscience · 2026Review
- Reframing macrophage polarization through cholesterol efflux: an organelle-coupled immunometabolic model.Frontiers in immunology · 2026Review
- The IRE1α Pathway Links Endoplasmic Reticulum Stress to Atherosclerosis-Related Inflammation and Lipid Accumulation.Mediators of inflammation · 2026Article
- Intracellular Calcium as a Regulator of Polarization and Target Reprogramming of Macrophages.International journal of molecular sciences · 2025Review
- TRIB3 Links Endoplasmic Reticulum Stress to Impaired Efferocytosis in Atherosclerosis.Circulation research · 2025Article
- Ensnarement of Stressed Macrophages by NETs in Atherosclerosis.Circulation research · 2025Article
- Micro-nanoplastic induced cardiovascular disease and dysfunction: a scoping review.Journal of exposure science & environmental epidemiology · 2025Article
- Anti-Atherogenic Mechanisms and Therapies.Current atherosclerosis reports · 2025Review
- How Do Organelle-Targeting Nanotherapeutics Treat Inflammatory Diseases? A Comprehensive Review of the Literature.International journal of nanomedicine · 2025Review
- Endoplasmic reticulum-associated degradation mitigates atherosclerosis by maintaining cellular homeostasis.Frontiers in physiology · 2025Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
The endoplasmic reticulum (ER) stress is an important event in the pathogenesis of different human disorders, including atherosclerosis. ER stress leads to disturbance of cellular homeostasis, apoptosis, and in the case of macrophages, to foam cell formation and pro-inflammatory cytokines production. In atherosclerosis, several cell types can be affected by ER stress, including endothelial cells, vascular smooth muscular cells, and macrophages. Modified low-density lipoproteins (LDL) and cytokines, in turn, can provoke ER stress through different processes. The signaling cascades involved in ER stress initiation are complex and linked to other cellular processes, such as lysosomal biogenesis and functioning, autophagy, mitochondrial homeostasis, and energy production. In this review, we discuss the underlying mechanisms of ER stress formation and the interplay of lipid accumulation and pro-inflammatory response. We will specifically focus on macrophages, which are the key players in maintaining chronic inflammatory milieu in atherosclerotic lesions, and also a major source of lipid-accumulating foam cells.
Indexed as
Identifiers
What OpenQuestion holds
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.