Key result
Review summarizes the phenotypic identification of adipose precursors and signals regulating their pathophysiological fate.
Why the study?
Adipose precursors and their fate decisions are only recently being defined to decipher how adipose tissues generate, maintain, and remodel.
This review highlights the mechanisms of adipose precursor fate determination, providing insights that may lead to novel therapeutic strategies for obesity and related metabolic diseases.
This is the authors' abstract. We don't add key points for this paper.
Adipose tissues are essential for actively regulating systemic energy balance, glucose homeostasis, immune responses, reproduction, and longevity. Adipocytes maintain dynamic metabolic needs and possess heterogeneity in energy storage and supply. Overexpansion of adipose tissue, especially the visceral type, is a high risk for diabetes and other metabolic diseases. Changes in adipocytes, hypertrophy or hyperplasia, contribute to the remodeling of obese adipose tissues, accompanied by abundant immune cell accumulation, decreased angiogenesis, and aberrant extracellular matrix deposition. The process and mechanism of adipogenesis are well known, however, adipose precursors and their fate decision are only being defined with recent information available to decipher how adipose tissues generate, maintain, and remodel. Here, we discuss the key findings that identify adipose precursors phenotypically, with special emphasis on the intrinsic and extrinsic signals in instructing and regulating the fate of adipose precursors under pathophysiological conditions. We hope that the information in this review lead to novel therapeutic strategies to combat obesity and related metabolic diseases.
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May guide obesity therapies targeting adipose precursors; leaves open clinical validation in trials.
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Ye et al. (2023) conducted a review in Obesity and related metabolic diseases. This review summarizes key findings on the phenotypic identification of adipose precursors and the intrinsic and extrinsic signals regulating their fate under pathophysiological conditions.
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