ReviewCurrent obesity reports2026
Pathophysiological Roles of Obesity-Induced Alterations in Extracellular Vesicles Derived from Adipose Tissue and Adipocytes.
Review in Current obesity reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Lipid Metabolic Disorders: a Pivotal Driver in Type 2 Diabetes Mellitus Pathogenesis.Current obesity reports · 2026Review
- Unlocking beta cell health: The clinical potential of extracellular vesicles in type 1 diabetes.Clinical and translational medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
purpose of reviewThis review aims to summarize current knowledge of the alterations and pathophysiological roles of adipose tissue (AT)-derived extracellular vesicles (AT-EVs) and adipocyte-derived EVs (Ad-EVs) in the context of obesity, while providing mechanistic insights into their potential functions within the tumor microenvironment. RECENT
findingsEmerging evidence indicates that obese AT-EVs and Ad-EVs contribute to insulin resistance, diabetes, metabolic dysfunction-associated steatotic liver disease, cardiovascular disorders, and cancer by delivering pathological cargo or altering recipient cell signaling. Conversely, both lean and obese AT-EVs and Ad-EVs have demonstrated therapeutic potential in specific settings, such as restoring insulin sensitivity, enhancing β-cell function, improving wound healing, and mitigating ischemia/reperfusion injury. One of the most prominent features of obesity is AT remodeling, which markedly increases the release of EVs and alters their cargo composition. These EVs can play context-dependent roles in pathophysiological processes, underscoring the complexity of AT-EV and Ad-EV biology and highlighting the need for further mechanistic investigations, particularly in cancer, where evidence remains limited. Advancing our understanding of the molecular pathways underlying their biogenesis, cargo sorting, and intercellular communication will not only deepen our knowledge of obesity-related pathophysiology but also facilitate the development of novel biomarkers and EV-based therapeutic strategies.
Indexed as
Identifiers
41543653What 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.