ArticleOpen life sciences2025
Iron overloaded M0 macrophages regulate hematopoietic stem cell proliferation and senescence via the Nrf2/Keap1/HO-1 pathway.
Article in Open life sciences, 2025. 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous studies have established a link between iron overload and hematological disorders, yet its impact on hematopoietic stem cell (HSCs) homeostasis remains unclear. This study investigates the effects of iron-overloaded macrophages on HSCs proliferation and senescence, focusing on the potential protective role of the Nrf2/Keap1/HO-1 signaling pathway. In this experiment, THP-1 cells were first differentiated into M0 macrophages, which were then exposed to ferric ammonium citrate (FAC) to establish an iron overload model. The impact of iron overload on macrophage function was assessed by measuring phagocytic activity, reactive oxygen species (ROS) levels, and inducible nitric oxide synthase (iNOS) expression. A co-culture system with HSCs was used to evaluate the effects of iron-overloaded macrophages on HSCs proliferation, cell cycle progression, and senescence. Western blot analysis was employed to measure oxidative stress and aging markers. Nrf2 activation was induced to assess its protective role. The results showed that iron overload significantly impaired macrophage function, as evidenced by reduced phagocytic activity, increased ROS production, and elevated iNOS expression. In the co-culture system, iron-overloaded macrophages inhibited HSCs proliferation, induced cell cycle arrest, and accelerated senescence, as evidenced by increased aging markers (P16, SA-β-gal) and decreased proliferative markers (HOXB4, RUNX1). Nrf2 activation with 2-trifluoromethyl-2'-methoxychalcone (TMC) reversed these effects, restoring HSCs proliferation and reducing oxidative damage. In conclusion, this study explores how iron-overloaded macrophages affect HSCs through the Nrf2/Keap1/HO-1 pathway.
Indexed as
Identifiers
What Socratic 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 Socratic graph.