PARP inhibition protects mitochondria and reduces ROS production via PARP-1-ATF4-MKP-1-MAPK retrograde pathway - ScienceDirect

PARP1 mediated PARylation contributes to myogenic progression and glucocorticoid transcriptional response

Time-dependent replicative senescence vs. disturbed flow-induced pre-mature aging in atherosclerosis - ScienceDirect

Reduction in mitochondrial ROS improves oxidative phosphorylation and provides resilience to coronary endothelium in non-reperfused myocardial infarction

PARP inhibition induces Akt-mediated cytoprotective effects through the formation of a mitochondria-targeted phospho-ATM-NEMO-Akt-mTOR signalosome - ScienceDirect

IJMS, Free Full-Text

Nucleus-mitochondria positive feedback loop formed by ERK5 S496 phosphorylation-mediated poly (ADP-ribose) polymerase activation provokes persistent pro-inflammatory senescent phenotype and accelerates coronary atherosclerosis after chemo-radiation

Synthesis and biological evaluation of gold(III) Schiff base complexes for the treatment of hepatocellular carcinoma through attenuating TrxR activity - ScienceDirect

PARP inhibition protects mitochondria and reduces ROS production via PARP-1- ATF4-MKP-1-MAPK retrograde pathway - ScienceDirect

Flavonoids from Rosa roxburghii Tratt prevent reactive oxygen species-mediated DNA damage in thymus cells both combined with and without PARP-1 expression after exposure to radiation in vivo - Figure f7

Sensing, signaling and surviving mitochondrial stress

The potential roles of ATF family in the treatment of Alzheimer's disease - ScienceDirect

Role of PARP-1 in mitochondrial homeostasis - ScienceDirect

p53 at the crossroad between mitochondrial reactive oxygen species and necroptosis - ScienceDirect

Nucleus-mitochondria positive feedback loop formed by ERK5 S496 phosphorylation-mediated poly (ADP-ribose) polymerase activation provokes persistent pro-inflammatory senescent phenotype and accelerates coronary atherosclerosis after chemo-radiation