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These findings are supported by gene expression data indicating upregulation of lipolytic markers and 3-adrenergic receptor transcripts

As previously mentioned, proof-of-concept came in 2008, when intra-ovarian BM-MSC transplantation in cyclophosphamide-injured rats restored estrous cycling, increased estrogen production and rebuilt follicular architecture, establishing that paracrine support from these cells can revive a depleted ovary [167]

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Furthermore, SFN orchestrates a multi-pronged assault on cancer cells by promoting the acetylation of non-histone proteins such as p53, and synergistically activating critical pathways including cell cycle arrest, apoptosis, and sensitization to other therapeutic agents like TRAIL, which is particularly promising for targeting therapy-resistant cases (66)