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GOT administration and endogenous up-regulation reduce infarct size in preclinical models of ischemic strokeGOT Treatment Shows Potential to Reduce Stroke Damage in Mice

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Key Takeaway
Note that GOT treatment reduces infarct size in rodent models, though results are limited by publication bias.

This meta-analysis synthesizes preclinical data regarding the effects of endogenous GOT up-regulation and exogenous GOT administration in rodent models of ischemic stroke. The primary outcome, infarct size, showed a significant reduction with an effect size of SMD = 1.14 (95% CI 0.61-1.67, p < 0.0001). Secondary outcomes, including edema, neuronal death, somatosensory evoked responses, and neurofunctional scores, were also reported as improved following GOT intervention.

Several limitations were identified in the pooled data. After publication bias correction, the effect size for infarct size was reduced by 28%. Furthermore, some functional outcomes lost statistical significance following this correction. The authors also noted that the included studies lacked diversity in animal models, specifically lacking female, aged, and comorbid animals.

While these findings suggest a therapeutic potential for GOT in the management of acute stroke, clinical translation is currently limited. The lack of diverse animal models in the primary data limits the generalizability of these results to human populations with varying ages, sexes, and comorbidities.

This study looked at how a substance called glutamate-oxaloacetate transaminase, or GOT, affects the brain after an ischemic stroke. Researchers tested this in mice and rats to see if it could limit damage and improve physical recovery. The study was a meta-analysis of previous laboratory results.

In the animal models, giving GOT or increasing its natural levels led to smaller stroke lesions and less brain swelling. The animals also showed improved nerve responses and better overall physical scores. These results suggest that GOT could be a promising target for future medical treatments for stroke patients.

Because this research was conducted only in mice and rats, the results cannot be applied directly to humans yet. The study also lacked data from female, older, or sick animals. While the findings are promising for the future of stroke care, more human clinical trials are needed to determine if this treatment is safe and effective for people.

What this means for you:
Early animal studies show GOT may reduce stroke damage, but more human research is needed to confirm its safety.

Common questions

What did the study find about stroke damage?

The study found that GOT treatment led to a reduction in infarct size and improved brain swelling. It also showed improvements in nerve responses and overall physical scores in the animal models. These results suggest that GOT has potential to help protect brain tissue after a stroke.

Is this treatment safe for humans?

This study was conducted only in mice and rats, so it does not provide information on human safety. Because it was a preclinical study, it cannot be used to determine if the treatment is safe or effective for people. You should talk to a doctor regarding stroke treatments.

Why are the results not yet used in hospitals?

The findings are currently limited to animal models. The study did not include female, aged, or comorbid animals, which are important for understanding how humans would react. More clinical trials are needed before this can be used as a standard medical treatment.

Study Details

Study typeMeta analysis
EvidenceLevel 1
PublishedNov 2026
View Original Abstract ↓
While independent preclinical studies have reported beneficial effects of glutamate-oxaloacetate transaminase (GOT) in models of ischemic stroke, these findings remain dispersed across the literature. This PRISMA-compliant systematic review and meta-analysis aims to combine data from these studies to determine GOT's therapeutic potential in ischemic stroke, focusing on the effects on lesion size and neurofunctional deficit. After screening results from searches in PubMed and Web of Science, and citation chasing, 12 eligible studies were included. Range of evidence met nine out of 13 STAIR criteria. Median (Q1, Q3) quality score was 8.5 (6, 11.25) on the CAMARADES 15-item checklist. Both endogenous GOT up-regulation and exogenous GOT administration reduced infarct size, with SMD = 1.14 (95% CI 0.61-1.67;  < 0.0001), to a higher extent in mice than in rats. GOT interventions also improved edema, neuronal death, somatosensory evoked responses and neurofunctional score. The findings support the therapeutic potential of GOT for acute stroke. However, effect sizes were substantially reduced after publication bias correction (28% reduction for infarct size, with some functional outcomes losing significance), and the complete absence of female, aged, and comorbid animals limits clinical translation. High-quality, pre-registered studies in clinically relevant populations are essential before clinical trials.
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