ArticleMolecular biology reports2026
Ex vivo modulation of monocyte/macrophage phenotypes by all-trans retinoic acid in chemotherapy-induced peripheral neuropathy.
Article in Molecular biology reports, 2026. 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
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChemotherapy-induced peripheral neuropathy (CIPN) is a common and debilitating complication associated with chemotherapeutic agents such as paclitaxel, oxaliplatin, and cisplatin. Persistent inflammation and oxidative stress are key contributors to neuronal damage in CIPN. All-trans retinoic acid (ATRA) possesses antioxidant and immunomodulatory properties, suggesting potential therapeutic value in modulating immune cell responses in CIPN.
methodsPeripheral blood mononuclear cells (PBMCs) were isolated from peripheral blood of eight patients with CIPN, and CD14⁺ monocytes were purified using fluorescence-activated cell sorting. Monocytes were treated with different concentrations of ATRA, and cell viability and apoptosis were evaluated using MTT and Annexin V-FITC/PI assays. Expression of inflammation-associated microRNAs was measured using qRT-PCR. Cytokine levels and antioxidant enzyme activities (superoxide dismutase and catalase) were assessed using ELISA. Monocytes were differentiated into macrophages using M-CSF, and macrophage polarization was evaluated using CD86 (M1) and CD206 (M2) markers. Additionally, apoptosis-related proteins and inflammatory signaling markers were analyzed by flow cytometry.
resultsATRA inhibited monocyte proliferation and induced apoptosis. Treatment increased anti-inflammatory microRNAs (miR-144-5p and miR-125b) while suppressing pro-inflammatory miR-155. ATRA reduced pro-inflammatory cytokine levels, enhanced anti-inflammatory mediator production, and increased antioxidant enzyme activity. Furthermore, ATRA promoted macrophage polarization toward the anti-inflammatory M2 phenotype and modulated apoptosis- and inflammation-related signaling proteins.
conclusionsATRA regulates inflammation-associated microRNAs, reduces pro-inflammatory cytokine expression, enhances antioxidant defenses, and promotes M2 macrophage polarization. These findings suggest that ATRA can shift monocyte and macrophage function toward a potentially protective, anti-inflammatory phenotype, contributing to the development of future therapeutic strategies for CIPN.
Indexed as
Identifiers
42363989What 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.