The short ACE2 isoform is upregulated in adipose tissue from women with obesity.
Salazar M., Teixeira D., Oliveira SM., Saraiva F., Pinho C., Jarnalo M.
Laboratory Study, published in Int J Obes (Lond) (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Int J Obes (Lond) (2026)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42527623
- DOI
- 10.1038/s41366-026-02177-1
Abstract (original English)
Background/objectives A novel short ACE2 isoform, lacking the SARS-CoV-2 binding domain and upregulated by interferons, was recently identified in human respiratory epithelia, spermatozoa, liver, and gastrointestinal and urogenital tracts. This study is the first to describe its presence in human adipose tissue (AT). Subjects/methods AT samples were collected from middle-aged women without obesity in subcutaneous regions-abdominal superficial, abdominal deep, and thigh-as well as from the visceral epiploon. Subcutaneous abdominal AT was also obtained from middle-aged women with previous obesity and from older women with and without obesity. Short ACE2 expression was determined by immunohistochemistry and Western blotting in AT, mature adipocytes, and stromal vascular fraction (SVF). Results Short ACE2 showed comparable expression in both subcutaneous and visceral AT, with enrichment in adipocytes. In contrast, full-length ACE2 displayed a different pattern, as its levels did not significantly differ between the SVF and adipocytes. Moreover, short ACE2 levels were higher in AT from women with obesity compared with those without obesity. Interestingly, short ACE2 expression was also elevated in AT from women with previous obesity. Conclusions Given that short ACE2 expression is induced by interferons, its upregulation in AT under obesity may reflect the interferon-enriched inflam
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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