Adipose Tissue Plasticity in Response to Pathophysiological Cues: A Connecting Link between Obesity and Its Associated Comorbidities.
Level 5 - mechanism / opinion, no new human data
Narrative review of biological mechanisms without systematic methodology or primary human data
PubMed 35628322 · doi:10.3390/ijms23105511
What was done
This is a narrative review synthesizing literature on adipose tissue plasticity and remodeling in response to energy balance variations. The authors examine the mechanistic processes linking adipose organ dysfunction to metabolic and cardiovascular complications, focusing on adipocyte precursor failure, hypertrophy, impaired redox homeostasis, low-grade inflammation, and cellular senescence.
What was found
The abstract provides a conceptual synthesis without quantitative data or statistical measurements. It describes a mechanistic model where limited adipose expandability triggers a triad of lipoxidation, inflammation, and cellular senescence, promoting ectopic lipid overspill (lipotoxicity) and altered adipokine and lipokine secretion.
Why it matters
It emphasizes that impaired adipose tissue plasticity and functional remodeling—rather than fat mass enlargement alone—drive obesity-associated cardiometabolic disease, presenting adipose plasticity as a potential therapeutic target.
Limits
As a non-systematic narrative review, the paper presents no original empirical data, quantitative meta-analysis, or predefined search criteria. The mechanistic frameworks described in the abstract are not supported by reported clinical sample sizes or statistical effect estimates.
Cited by
- supports Adipose tissue becomes pro-inflammatory when it exceeds a certain threshold.