ArticleNature communications2026
Bnip3lb-driven mitophagy maintains fate of the embryonic hematopoietic stem cell pool.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Mitophagy-driven prognosis in pediatric acute myeloid leukemia: a new frontier.Scientific reports · 2026Article
- Mitochondrial quality control in hematopoietic stem cells: mechanisms, implications, and therapeutic opportunities.Stem cell research & therapy · 2025Review
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Authors and funding
20 authors.
Funding
Abstract
Embryonic hematopoietic stem and progenitor cells (HSPCs) have the clinically valuable ability to undergo substantial proliferative expansion while maintaining multipotency, which remains difficult to replicate in culture. Here, we show that newly specified HSPCs achieve this unique state by precise spatio-temporal regulation of reactive oxygen species (ROS) via Bnip3lb-associated developmentally-programmed mitophagy, a distinct autophagic regulatory mechanism from that of adult HSPCs. While ROS drives HSPC specification in the dorsal aorta, scRNAseq and live-imaging of mitophagy-reporter zebrafish indicate that mitophagy initiates during endothelial-to-hematopoietic transition and colonization of secondary niches. Knockdown of bnip3lb reduces mitophagy and HSPC numbers in the caudal hematopoietic tissue by promoting myeloid-biased differentiation and apoptosis, which can be rescued by antioxidant exposure. Conversely, chemical or genetic induction of mitophagy enhances embryonic HSPC and lymphoid progenitor numbers. Significantly, compound-mediated mitophagy activation improves ex vivo function of HSPCs derived from human-induced pluripotent stem cells, enhancing serial-replating hematopoietic colony forming potential.
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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 Socratic graph.