Autophagy in traumatic brain injury: a new target for therapeutic intervention
Open accessAbstract
Traumatic brain injury (TBI) is one of the most devastating forms of brain injury. Many pathological mechanisms such as oxidative stress, apoptosis and inflammation all contribute to the secondary brain damage and poor outcomes of TBI. Current therapies are often ineffective and poorly tolerated, which drive the explore of new therapeutic targets for TBI. Autophagy is a highly conserved intracellular mechanism during evolution. It plays an important role in elimination abnormal intracellular proteins or organelles to maintain cell stability. Besides, autophagy has been researched in various models including TBI. Previous studies have deciphered that regulation of autophagy by different molecules and pathways could exhibit anti-oxidative stress, anti-apoptosis and anti-inflammation effects in TBI. Hence, autophagy is a promising target for further therapeutic development in TBI. The present review provides an overview of current knowledge about the mechanism of autophagy, the frequently used methods to monitor autophagy, the functions of autophagy in TBI as well as its potential molecular mechanisms based on the pharmacological regulation of autophagy.
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Exopher formation and extracellular proteostasis have been discovered in recent years.
“Newer mechanisms to manage proteostasis, such as exopher formation and extracellular proteostasis, have been discovered in recent years.165,166”
From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [166]
The Methods for Monitoring Autophagy and FoxO3a passages discuss intracellular autophagy, not exopher formation or extracellular proteostasis. Searches of our full-text copy for both terms found no passage addressing their discovery; the supplied passages have no page numbers. (LLM, conf=0.76)
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- Authors
- Zhang, L., & Wang, H.
- Affiliations
- Nanjing General Hospital of Nanjing Military Command (CN)
- Corresponding author
- Wang, Handong
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2018-06-05
- Volume
- 11
- Pages
- 190-190
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC5996030
- OpenAlex
- W2807583409
- Cited by
- 82
- References
- 167
- Citations by year
- 2025: 11 · 2024: 13 · 2023: 14 · 2022: 12 · 2021: 7 · 2020: 13 · 2019: 11 · 2018: 1
- FWCI
- 1.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Molecular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81672503, 81702484)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Keywords
- autophagy, traumatic brain injury, secondary brain injury, oxidative stress, apoptosis, neuroinflammation, autophagy regulation, autophagy monitoring, therapeutic target
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