ArticleCell death & disease2026
CD5L promotes efferocytosis and resolution of retinal ischemic injury.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Ischemia-induced retinopathy is a defining feature of prevalent ocular conditions, including diabetic retinopathy and central retinal artery or vein occlusion. Therapeutic interventions for ischemic retinopathies show limited efficacy and adverse effects, highlighting the need to thoroughly investigate the underlying mechanisms. Histone deacetylase 3 (HDAC3), a member of the histone deacetylase family, plays a central role in regulating gene expression in myeloid cells (microglia and macrophages). We recently showed that myeloid HDAC3 deletion promotes tissue repair and functional recovery after retinal ischemia-reperfusion (IR) injury via efferocytosis, a process by which myeloid cells engulf and clear apoptotic cells. Here, we investigated the mechanism by which myeloid HDAC3 deletion enhances efferocytosis. Employing an in vitro efferocytosis assay coupled with RNA sequencing on HDAC3 KO macrophages revealed that the secreted protein, CD5 molecule-like (CD5L), was the most upregulated among other pro-efferocytic genes. In vivo, we found that CD5L levels markedly increased in the retinas of myeloid HDAC3 KO mice subjected to IR injury, and its expression colocalized with myeloid cells. Co-immunoprecipitation experiments showed that HDAC3 represses CD5L expression in a liver X receptor (LXRα)-dependent manner. Additionally, we found that CD36, a receptor for CD5L that facilitates the clearance of apoptotic cells, was upregulated in retinal myeloid cells after IR. In vitro, CD5L treatment enhanced efferocytosis via CD36. We then evaluated the role of CD5L in retinal IR injury using in vivo neuronal, vascular, structural, and functional endpoints. CD5L KO mice showed worsened outcomes after IR, whereas treatment with recombinant CD5L was protective against retinal ischemic injury. Collectively, our findings suggest that deleting HDAC3 enhances macrophage efferocytosis by upregulating the CD5L/CD36 axis. CD5L may serve as a promising therapeutic target to improve outcomes in ischemic retinopathy.
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.