ArticleBiotechnology progress2026
Lipid droplet profiling during neutrophil differentiation by stimulated Raman scattering microscopy.
Article in Biotechnology progress, 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
6 authors.
Funding
Abstract
Lipid droplets (LDs) are dynamic organelles that serve as metabolic hubs and emerging regulators of immune cell fate. Although LDs have been implicated in immune regulation, how LD metabolism is remodeled during neutrophil differentiation and how stage-specific LD dynamics shape mature neutrophil function remain poorly defined. Here, we profiled LD dynamics during neutrophil development and evaluated their role in innate immune function. Using stimulated Raman scattering (SRS) microscopy, we performed label-free, quantitative mapping of LD accumulation in two complementary differentiation systems: murine Hoxb8 myeloid progenitors and human pluripotent stem cell (hPSC)-derived neutrophils. To define metabolic requirements, we pharmacologically modulated LD biosynthesis and catabolism throughout neutrophil differentiation. Perturbing LD metabolism did not impair differentiation efficiency or lineage commitment, but significantly altered the functional output of mature neutrophils. In the murine system, inhibition of adipose triglyceride lipase (ATGL)-mediated LD breakdown enhanced reactive oxygen species (ROS) production and increased anti-tumor cytotoxicity against GL261 glioma cells. In the hPSC model, ATGL inhibition during the myeloid progenitor-to-neutrophil transition selectively increased intracellular LD accumulation without compromising neutrophil yield or purity. This metabolic rewiring also elevated ROS production in hPSC-derived neutrophils, although cytotoxic enhancement against U87MG glioblastoma cells was less pronounced than in the murine system. Collectively, these findings define a stage-specific LD metabolic landscape during neutrophil development and highlight targeted LD modulation as a potential strategy to enhance the functional potency of therapeutic neutrophils.
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.