Neuroprotective and neurorestorative effects of thymosin β4 treatment following experimental traumatic brain injury
Open accessAbstract
Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. No effective pharmacological treatments are available for TBI because all phase II/III TBI clinical trials have failed. This highlights a compelling need to develop effective treatments for TBI. Endogenous neurorestoration occurs in the brain after TBI, including angiogenesis, neurogenesis, synaptogenesis, oligodendrogenesis, and axonal remodeling, which may be associated with spontaneous functional recovery after TBI. However, the endogenous neurorestoration following TBI is limited. Treatments amplifying these neurorestorative processes may promote functional recovery after TBI. Thymosin beta 4 (Tβ4) is the major G-actin-sequestering molecule in eukaryotic cells. In addition, Tβ4 has other properties including antiapoptosis and anti-inflammation, promotion of angiogenesis, wound healing, stem/progenitor cell differentiation, and cell migration and survival, which provide the scientific foundation for the corneal, dermal, and cardiac wound repair multicenter clinical trials. Here, we describe Tβ4 as a neuroprotective and neurorestorative candidate for treatment of TBI.
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MD5828-specific microglial factor 5 had high loadings of TMSB4X and CSF1R, genes important in acute TBI response.
“the MD5828- specific metagene for factor 5, which was microglia-specific, had high loadings of TMSB4X and CSF1R, both of which play important roles in the acute response to TBI (Luo et al., 2013; Xiong et al., 2012).”
From Single-Cell Multi-omic Integration Compares and Contrasts Features of Brain Cell Identity (2019) · cites this paper as Xiong et al., 2012
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Single-Cell Multi-omic Integration Compares and Contrasts Features of Brain Cell Identity
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- Authors
- Xiong, Y., Mahmood, A., Meng, Y., Zhang, Y., Zhang, Z. G., Morris, D. C., & Chopp, M.
- Affiliations
- Henry Ford Health (US)
- Corresponding author
- Xiong, Ye
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2012-10
- Volume
- 1270
- Issue
- 1
- Pages
- 51-58
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- PMC
- PMC3547647
- OpenAlex
- W1542991608
- Cited by
- 44
- References
- 87
- Citations by year
- 2025: 2 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 3 · 2019: 6 · 2018: 7 · 2017: 2 · 2016: 6 · 2015: 8 · 2014: 2 · 2013: 2
- FWCI
- 2.51
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG038648)
- National Institute of Neurological Disorders and Stroke (R01NS062002, P01NS023393, P01NS42345, R01 NS 62002, P01NS042345)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Keywords
- thymosin beta 4, traumatic brain injury, neuroprotection, neurorestoration, functional recovery, angiogenesis, neurogenesis, oligodendrogenesis, axonal remodeling, apoptosis inhibition, anti-inflammation, wound healing
- MeSH terms
- Thymosin beta(4), Animals, Brain Injuries, Humans, Thymosin, Wound Healing, Neovascularization, Physiologic, Rats, Neurogenesis
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