ArticleInternational journal of molecular sciences2023
Endoplasmic Reticulum Stress Causing Apoptosis in a Mouse Model of an Ischemic Spinal Cord Injury.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- The influence of exercise duration on inhibiting endoplasmic reticulum stress in ischemic stroke rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- Establishment and multifaceted characterization of a graded spinal cord injury model based on graduated impact depth.Animal models and experimental medicine · 2026Article
- Endoplasmic reticulum stress-mediated cell death in spinal cord injury: from molecular mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2026Review
- Integrative analysis identifies Hspa5 as a key regulator of the ERS/UPR-immune axis in spinal cord injury.Frontiers in genetics · 2026Article
- Dimethyloxalylglycine improves functional recovery through inhibiting cell apoptosis and enhancing blood-spinal cord barrier repair after spinal cord injury.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2025Article
- Spinal cord injury models: Advantages and disadvantages in the view of pathophysiology and clinical significance.Biochemistry and biophysics reports · 2025Review
- The Interplay Between Endoplasmic Reticulum Stress and Ferroptosis in Neurological Diseases.Neurochemical research · 2025Review
- Tyrosine Kinase Inhibitor Lenvatinib Causes Cardiotoxicity by Inducing Endoplasmic Reticulum Stress and Apoptosis through Activating ATF6, IRE1α and PERK Signaling Pathways.Recent patents on anti-cancer drug discovery · 2025Article
- Neuroprotective Effects of Chaperonin Containing TCP1 Subunit 2 (CCT2) on Motor Neurons Following Oxidative or Ischemic Stress.Neurochemical research · 2024Article
- Chronic Corticosterone Administration-Induced Mood Disorders in Laboratory Rodents: Features, Mechanisms, and Research Perspectives.International journal of molecular sciences · 2024Review
- The effects of resistance training on cardiovascular factors and anti-inflammation in diabetic rats.Heliyon · 2024Article
- Feasibility exploration of GSH in the treatment of acute hepatic encephalopathy from the aspects of pharmacokinetics, pharmacodynamics, and mechanism.Frontiers in pharmacology · 2024Article
- The time-dependent changes in a mouse model of traumatic brain injury with motor dysfunction.PloS one · 2024Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
A spinal cord injury (SCI) is the devastating trauma associated with functional deterioration due to apoptosis. Most laboratory SCI models are generated by a direct impact on an animal's spinal cord; however, our model does not involve the direct impact on the spinal cord. Instead, we use a clamp compression to create an ischemia in the descending aortas of mice. Following the success of inducing an ischemic SCI (ISCI), we hypothesized that this model may show apoptosis via an endoplasmic reticulum (ER) stress pathway. This apoptosis by the ER stress pathway is enhanced by the inducible nitric oxide synthase (iNOS). The ER is used for the protein folding in the cell. When the protein folding capacity is overloaded, the condition is termed the ER stress and is characterized by the accumulation of misfolded proteins inside the ER lumen. The unfolded protein response (UPR) signaling pathways that deal with the ER stress response then become activated. This UPR activates the three signal pathways that are regulated by the inositol-requiring enzyme 1α (IRE1α), the activating transcription factor 6 (ATF6), and the protein kinase RNA-like ER kinase (PERK). IRE1α and PERK are associated with the expression of the apoptotic proteins. Apoptosis caused by an ISCI is assessed using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) test. An ISCI also reduces synaptophysin and the neuronal nuclear protein (NeuN) in the spinal cord. In conclusion, an ISCI increases the ER stress proteins, resulting in apoptosis in neuronal cells in the spinal cord.
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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.