Adipose Tissue Stromal Cells: Rheostats for Adipose Tissue Function and Metabolic Disease Risk.
Scheidl TB., Wager JL., Thompson JA.
Narrative Review on Chronic Inflammation, published in Can J Cardiol (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
- Narrative Review
- Journal
- Can J Cardiol (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 39986382
- DOI
- 10.1016/j.cjca.2025.02.025
Abstract (original English)
The transition from metabolically healthy obesity to the development of obesity-associated metabolic syndrome and cardiovascular disease is thought to be triggered by a loss in the functional integrity of adipose tissue. Although mature adipocytes are the primary functional units that carry out lipid partitioning in adipose tissue for the promotion of whole-body energy balance, they are supported by a heterogenous collection of nonadipocytes in the stroma. Research over the past couple of decades has expanded perspectives on the homeostatic and pathological roles of the nonadipocyte compartment. Adipose progenitors originate in the embryonic period and drive the developmental adipogenesis that establishes the set point of adiposity. A population of adipocyte progenitors reside in adult depots and serve an important homeostatic role as a reservoir to support adipocyte turnover. Adipocyte hypertrophy in obesity increases the rate of adipocyte death and the ability of progenitors to support this high rate of adipocyte turnover is important for the preservation of the lipid-buffering function of adipose tissue. Some evidence exists to suggest that impaired adipogenesis or a decline in progenitors capable of differentiation is a key event in the development of adipose dysfunction. The efficiency of macrophages to clear the debris and toxic lipids released from dead adipocytes lies a
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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