Perivascular Adipocytes' Adipogenesis Is Defined by Their Anatomical Location in the Descending Thoracic Aorta.
Contreras GA., Rendon CJ., Shadowens A., Chirivi M., Salcedo-Tacuma D., Lauver DA.
Animal Study with a reported sample of 7, published in Cells (2025) — 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
- Animal Study
- Journal
- Cells (2025)
- Country
- Switzerland
- Reported sample size
- 7
- Source database
- PubMed
- PMID
- 40277904
- PMCID
- PMC12026431
- DOI
- 10.3390/cells14080579
- Citations
- 2
Abstract (original English)
Cardiovascular diseases such as hypertension alter thoracic aorta structure. The role that the outer layer of the aorta, its perivascular adipose tissue (PVAT), plays in the pathogenesis of these alterations is poorly understood. In the descending thoracic aorta, PVAT is organized into three distinct strips: one located anterior to the aorta (AP) and two positioned laterally (LP). Genetic tracing indicates differences in the ontogeny of LP and AP, but the implications of these developmental differences and PVAT distribution on adipocyte development remain unknown. We hypothesize that the anatomical location of adipocyte progenitors influences their adipogenic potential and vasoactive functions. PVAT from LP and AP was collected from male SD rats at 10 wks of age (n = 7) to harvest adipocyte progenitors that were differentiated to adipocytes in adipogenic media. Adipogenesis was evaluated after induction and we performed next-generation RNA-seq on progenitors and adipocytes. We then employed Gene Set Enrichment Analysis for enrichment and network analyses. LP progenitors exhibited a 1.13-fold higher adipogenesis rate compared to those from AP. DEG analysis revealed LP had higher expression of adipogenic regulators and basal collagens Col4a2 and Col4a4 . When challenged with angiotensin-II, adipocyte progenitors from LP maintained their adipogenic capacity and adipocytes from the
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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