Magnetic-Field Induced First-Order Transition in the Frustrated XY Model on a Stacked Triangular Lattice

The results of extensive Monte Carlo simulations of magnetic-field induced transitions in the xy model on a stacked triangular lattice with antiferromagnetic intraplane and ferromagnetic interplane interactions are discussed. A low-field transition from the paramagnetic to a 3-state (Potts) phase is found to be very weakly first order with behavior suggesting tricriticality at zero field. In addition to clarifying some long-standing ambiguity concerning the nature of this Potts-like transition, the present work also serves to further our understanding of the critical behavior at $T_N$, about which there has been much controversy.Comment: 10 pages (RevTex 3.0), 4 figures available upon request, CRPS-93-0

Apoptotic stress causes mtDNA release during senescence and drives the SASP

Senescent cells drive age-related tissue dysfunction partially through the induction of a chronic senescence-associated secretory phenotype (SASP)1. Mitochondria are major regulators of the SASP; however, the underlying mechanisms have not been elucidated2. Mitochondria are often essential for apoptosis, a cell fate distinct from cellular senescence. During apoptosis, widespread mitochondrial outer membrane permeabilization (MOMP) commits a cell to die3. Here we find that MOMP occurring in a subset of mitochondria is a feature of cellular senescence. This process, called minority MOMP (miMOMP), requires BAX and BAK macropores enabling the release of mitochondrial DNA (mtDNA) into the cytosol. Cytosolic mtDNA in turn activates the cGAS–STING pathway, a major regulator of the SASP. We find that inhibition of MOMP in vivo decreases inflammatory markers and improves healthspan in aged mice. Our results reveal that apoptosis and senescence are regulated by similar mitochondria-dependent mechanisms and that sublethal mitochondrial apoptotic stress is a major driver of the SASP. We provide proof-of-concept that inhibition of miMOMP-induced inflammation may be a therapeutic route to improve healthspan