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[DOI] [PubMed] [Google Scholar] Said SI, Rosenberg RN

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This revealed both common and perturbation-specific aspects of the integrated stress-response to mtDNA depletion, that were only partially mediated by Atf4, and caused cell-cycle stage-independent slowing of cell proliferation

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Therefore, sphingolipid-autophagy crosstalk constitutes a pivotal regulatory nexus governing Treg stability, whose diabetic disruption propagates T1DM immunopathology by crippling immunosuppressive circuits, while pharmacologically restoring this axis emerges as a strategic therapeutic paradigm for re-establishing immune tolerance (Figure 5)

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