Investigation of the Mechanism by which GC Mediates the SLC25A10/HSL/SUCNR1 Pathway in Driving SLE-induced Adipose Tissue Remodeling, and Therapeutic Study of the Detoxification and Blood Stasis-Resolving Yin-Nourishing Formula
Abstract
Long-term glucocorticoid therapy in systemic lupus erythematosus (SLE) is prone to induce adipose tissue remodeling, though
the underlying mechanisms remain unclear. This study utilized a lupus-prone mouse model and primary adipocytes, combined with in vivo
modeling, gene silencing techniques, and mitochondrial function assays, to demonstrate that glucocorticoids upregulate SLC25A10, thereby
promoting succinate efflux, activating the SUCNR1 pathway to suppress hormone-sensitive lipase (HSL) activity, and exacerbating lipid metabolism disorders and inflammation. The "Detoxification and Blood Stasis-Resolving Yin-Nourishing Formula" targets SLC25A10 to repair
lipolysis and block inflammatory signaling; by preserving the anti-inflammatory efficacy of glucocorticoids, this formula ameliorates adipose
tissue remodeling, providing an experimental basis for interventions targeting glucocorticoid-induced metabolic toxicity.
the underlying mechanisms remain unclear. This study utilized a lupus-prone mouse model and primary adipocytes, combined with in vivo
modeling, gene silencing techniques, and mitochondrial function assays, to demonstrate that glucocorticoids upregulate SLC25A10, thereby
promoting succinate efflux, activating the SUCNR1 pathway to suppress hormone-sensitive lipase (HSL) activity, and exacerbating lipid metabolism disorders and inflammation. The "Detoxification and Blood Stasis-Resolving Yin-Nourishing Formula" targets SLC25A10 to repair
lipolysis and block inflammatory signaling; by preserving the anti-inflammatory efficacy of glucocorticoids, this formula ameliorates adipose
tissue remodeling, providing an experimental basis for interventions targeting glucocorticoid-induced metabolic toxicity.
Keywords
Systemic Lupus Erythematosus; Glucocorticoids; Adipocyte remodeling; SLC25A10; Detoxification and Blood Stasis-Resolving
Yin-Nourishing Formula
Full Text:
PDFReferences
[1] Sanz I, Lee FE. B cells as therapeutic targets in SLE[J]. Nature Reviews Rheumatology, 2010, 6(6): 326-337.
[2] Li H, Adamopoulos I E, Moulton V R, et al. Systemic lupus erythematosus favors the generation of IL-17 producing double negative T
cells[J]. Nature Communications, 2020, 11(1): 2859.
[3] Sun W, Li P, Cai J, Ma J, Zhang X, Song Y, Liu Y. Lipid Metabolism: Immune Regulation and Therapeutic Prospectives in Systemic Lupus Erythematosus. Front Immunol. 2022 Mar 18;13:860586.
[4] Yang ZH, Chen FZ, Zhang YX, Ou MY, Tan PC, Xu XW, Li QF, Zhou SB. Therapeutic targeting of white adipose tissue metabolic dysfunction in obesity: mechanisms and opportunities. MedComm (2020). 2024 May 24;5(6):e560.
DOI: http://dx.doi.org/10.70711/pmr.v3i11.10332
Refbacks
- There are currently no refbacks.
