ArticleBMC biology2025
Modification of adipose mass by targeting distal enhancers of Ptrf.
Article in BMC biology, 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
21 authors.
Funding
Abstract
backgroundAdipose tissue plays a central role in systemically metabolic regulation. Polymerase I and transcript release factor (PTRF) is responsible for caveolae structure formation and plays a crucial role in lipid metabolism.
resultsWe investigated the possibility of modifying adipose mass by targeting the enhancers of Ptrf. Single-nucleus transcriptomic analysis revealed that the reduction in fat mass caused by Ptrf knockout is associated with impaired adipogenesis and differentiation, adipocyte metabolism, nutrient transportation, and altered regulatory network. We demonstrated a closely positive association between Ptrf transcription and adipose mass in mice. Then, circular chromosome conformation capture sequencing and ChIP-seq data of mature adipocytes identified six candidate enhancers (E1-E6) of Ptrf, and the dual-luciferase reporting system revealed the transcriptional activity of three active candidate enhancers (E1, E3, E5) in Human embryonic kidney 293 (HEK293) and mouse embryo fibroblast (3T3-L1) cells. During the adipogenic differentiation of 3T3-L1, the epigenetic perturbation of these enhancers with the dCas9-KRAB system demonstrated their important roles during adipogenesis, with inhibited Ptrf expression and decreased lipid droplets and triglyceride contents. Injecting lentivirus carrying the dCas9-KRAB system into the inguinal fat of mice downregulated Ptrf expression and decreased body weight, body adipose percentage, and adipocyte diameter in vivo. Additionally, we observed the close binding of Pparg and Cebpa to Ptrf-E1.
conclusionsTaken together, these findings identify the mechanism by which Ptrf deletion leads to reduced fat mass in mice, and indicate that adipose mass may be reduced by targeting cis-regulatory elements of key adipogenesis-related genes.
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.