ArticleBone marrow transplantation2008
How lithium treatment generates neutrophilia by enhancing phosphorylation of GSK-3, increasing HIF-1 levels and how this path is important during engraftment.
Article in Bone marrow transplantation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05221593 (Evaluation of Lithium Efficacy Against Chemotherapy Induced Neutropenia in Breast Cancer Patients), which is not on this map. Cited by 4 papers.
What it found
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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.
Evaluation of Lithium Efficacy Against Chemotherapy Induced Neutropenia in Breast Cancer Patients
Who cites it
4 citing papers in PubMed, 30 citations in OpenAlex.
- Elraglusib and chemotherapy in metastatic pancreatic ductal adenocarcinoma: a randomized controlled phase 2 trial.Nature medicine · 2026Trial
- Effect of lithium on chemotherapy-induced neutropenia in Egyptian breast cancer patients; a prospective clinical study.Cancer chemotherapy and pharmacology · 2024Trial
- Pharmacological modulation of HIF-1 in the treatment of neuropsychiatric disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- The Roles of Exosomes upon Metallic Ions Stimulation in Bone Regeneration.Journal of functional biomaterials · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lithium is commonly used in psychiatry for mood stabilization. Lithium treatment results in neutrophilia, increased platelets and increased circulating CD34+ haematopoietic stem cells, HSC. This paper outlines the newly discovered mechanism by which this occurs. Glycogen synthase kinase-3, GSK-3, phosphorylates and thereby inactivates hypoxia-induced factor-1, HIF-1. HIF-1 is a transcription factor triggering transcription of multiple genes related to adaptation to hypoxia, among which is CXCL12. CXCL12 forms the primary homing gradient for CD34+ HSCs towards the hypoxic, trophic bone marrow niche to which they must go to thrive. Lithium inhibits GSK-3 thereby increasing active HIF-1 that results in a stronger CXCL12 homing gradient. Trophic niche function is enhanced, ultimately resulting in increased production of neutrophils, platelets and CD34+ cells. Sitagliptin is a new drug to treat diabetes that coincidentally inhibits destruction of CXCL12. Thus, lithium and sitagliptin enhance CXCL12 by different paths, potentially increasing trophic niche function. Awareness of this path is important in HSC transplantation.
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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 OpenQuestion graph.