ArticleBlood2025
Metabolic adaptation of regenerative hematopoiesis depends on docking-independent mitochondrial connexin 43.
Article in Blood, 2025. 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.
- Review
- Ferrostatin-1 and hinokitiol supplementation enhance human hematopoietic stem cell expansion in a chemically defined medium.Molecular therapy. Advances · 2026Article
Corrections and comments
- Commented on by
Authors and funding
10 authors.
Funding
Abstract
abstractHematopoietic stem cells (HSCs) exhibit a distinctive antioxidant profile during steady-state and stress hematopoiesis. HSCs and multipotential progenitors (MPPs) are metabolically coupled to bone marrow mesenchymal stromal cells through mitochondrial transfer, a process dependent on hematopoietic connexin 43 (Cx43) and low adenosine monophosphate-activated protein kinase (AMPK) activity. However, the mechanism by which Cx43 preserves mitochondrial functionality in HSCs remains elusive. Here, through integrated transcriptomic, proteomic, metabolomic, phenotypic, and functional analyses of HSCs and their isolated mitochondria, we identified that Cx43 is present on the inner and outer mitochondrial membranes of HSCs/MPPs, in which it primarily regulates mitochondrial metabolism and adenosine triphosphate synthesis by preserving the mitochondrial cristae, activation of mitochondrial AMPK, and 2-oxoglutarate dehydrogenase, a rate-liming enzyme in tricarboxylic acid cycle and electron transfer chain. During replicative stress, Cx43-deficient HSCs/MPPs fail to adapt metabolically and accumulate mitochondrial Ca2+, leading to increased mitochondrial AMPK activity, mitochondrial fission, mitophagy, and production of reactive oxygen species, thereby limiting HSC/MPP regeneration potential. Disruption of hyperfragmentation of mitochondria and mitophagy by Drp1 dominant-negative mutant (Drp1K38A) or restoration of mitochondrial function through ex vivo heteroplasmy prevents the harmful effects of Cx43 deficiency on mitochondrial metabolism and restore HSC activity in serial transplantation experiments. Re-expression analysis of Cx43 structure-function mutants indicates that Cx43 hemichannels are sufficient to reset HSC mitochondrial metabolism, dynamics, Ca2+ levels, and regeneration capacity. This report defines the cell-autonomous mechanism of action behind the role of Cx43 in HSC activity and opens a venue to translational applications in transplantation.
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.