Physiology articles from across Nature Portfolio

By parsing stimulus-responsive sources of astrocytic reactive oxygen species (ROS), Barnett et al. reveal how mitochondrial complex III-derived signals uniquely shape inflammatory responses and astrocyte–neuron crosstalk, linking mitochondrial redox cues to dementia-related neurodegeneration.

In cardiomyopathy caused by mutations in LMNA, which encodes the nuclear protein lamin A/C, cardiomyocyte nuclei are fragile and prone to rupture. This study reveals that this rupture arises from forces generated by a perinuclear microtubule cage, rather than from sarcomere contraction. Targeting microtubule–nuclei interactions might offer a therapeutic strategy to preserve cardiac function.

Yi and colleagues demonstrate that age-induced degradation of extracellular matrix generates elastin-derived fragments that activate the innate and adaptive immune system, which evokes systemic inflammaging.

Barbara Demmig-Adams discusses a 1998 study that demonstrated in plants that carotenoids can remove dangerous excess energy from chlorophyll, and the implications of this work, including for research aimed at improving plant stress resilience.

By parsing stimulus-responsive sources of astrocytic reactive oxygen species (ROS), Barnett et al. reveal how mitochondrial complex III-derived signals uniquely shape inflammatory responses and astrocyte–neuron crosstalk, linking mitochondrial redox cues to dementia-related neurodegeneration.

In cardiomyopathy caused by mutations in LMNA, which encodes the nuclear protein lamin A/C, cardiomyocyte nuclei are fragile and prone to rupture. This study reveals that this rupture arises from forces generated by a perinuclear microtubule cage, rather than from sarcomere contraction. Targeting microtubule–nuclei interactions might offer a therapeutic strategy to preserve cardiac function.