ReviewNeurochemical research2025
Advances in ERK Signaling Pathway in Traumatic Brain Injury: Mechanisms and Therapeutic Potential.
Review in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Neurotrophin System as a Complex Set of Potential Biomarkers in Psychiatric Disorders and Therapy-Overview of Recent Advances.International journal of molecular sciences · 2026Review
- The AMPK-BECN1-System Xc⁻ Pathway in Traumatic Brain Injury: Implications for Exosome-Based Therapy.Cellular and molecular neurobiology · 2026Review
- Astrocytes in neuroinflammation and brain cancer.Molecular biomedicine · 2026Review
- Roles of MAPKs, Including Those Activated by BDNF/TrkB, and Their Contribution in Neurodegenerative Diseases.International journal of molecular sciences · 2026Review
- Epidermal growth factor receptor modulation for neural repair: Implications for neurodegenerative disease therapy.Frontiers in molecular neuroscience · 2026Review
- Enhancing glymphatic transport through angiotensin II type 2 receptor activation promotes neurological recovery after traumatic brain injury.Theranostics · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) stands as one of the leading global causes of disability and mortality. Its pathological progression involves intricate secondary injury mechanisms, including oxidative stress, neuroinflammation, apoptosis, and ferroptosis. Current clinical treatments primarily focus on symptom management, yet lack effective intervention strategies targeting core pathological pathways. Recent studies have revealed that the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway plays a pivotal regulatory role in TBI-related secondary injuries. On one hand, the spatiotemporal-specific activation of ERK1/2 exerts neuroprotective effects by modulating neuronal survival, vascular repair, and glial cell phenotypic transformation. Conversely, its hyperactivation exacerbates oxidative damage, inflammatory cascades, and programmed cell death. This review systematically examines the dual roles and molecular mechanisms of the ERK1/2 pathway across distinct pathological processes post-TBI (e.g., apoptosis, autophagy, ferroptosis), while summarizing the neuroprotective efficacy of ERK-targeting pharmacological agents (e.g., tetrahydrocurcumin, ulinastatin) in animal models. These advancements, achieved through precise modulation of ERK pathway activity and functionality, offer novel directions for pathological intervention in TBI.
Indexed as
Identifiers
40489029What 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.