ArticleInvestigative ophthalmology & visual science2026
SIRT4 Alleviates Retinal Ischemia-Reperfusion Injury Via Mediating Astrocytes Lipid Metabolism and Mitochondrial Function.
Article in Investigative ophthalmology & visual science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: To investigate whether SIRT4 protects the optic nerve by regulating mitochondrial function and lipid metabolism in neurotoxic reactive astrocytes in the retinal ischemia-reperfusion injury. Methods: Using SIRT4 knockout, wild-type, and overexpressing mouse ischemia-reperfusion (I/R) models, we assessed retinal ganglion cell loss, protein expression (SIRT4, APOL6, GBP2, mitochondrial dynamics), and conducted metabolomic/transcriptomic analyses. In vitro, primary astrocytes were treated with TIC cytokines; SIRT4 was knocked down via lentivirus, followed by measurement of ATP, lipid secretion, and mitochondrial morphology/function. Results: SIRT4 was highly expressed in astrocytes. Its knockdown exacerbated I/R injury, promoting a neurotoxic astrocyte phenotype with increased APOL6 expression, and elevated secretion of long-chain fatty acids and phosphatidylcholines and mitochondrial damage. SIRT4 deficiency enhanced astrocyte susceptibility to injury, further reducing ATP production and worsening lipid accumulation and optic nerve damage. Conclusions: SIRT4 plays a protective role in retinal ischemia-reperfusion injury model by regulating astrocyte lipid metabolism and mitochondrial function, offering a potential therapeutic target for neuroprotection.
Indexed as
Identifiers
What 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.