Table 2.
Ppif−/− phenotypes in physiology.
| Pathology and Physiology of Ppif gene-deleted Mice | ||
|---|---|---|
| Mouse model | Phenotype as compared to WT controls | Reference |
| Myocardial IR | decreased infarct size | (5, 35) |
| Permanent LCA ligation (myocardial infarction) | increased survival, decreased scar size | (149) |
| transaortic constriction (pressure-overload heart failure) | increased pathology, decreased LV function | (95) |
| CamKIIδc-transgenic model (Ca2+-overload induced cardiomyopathy) | increased pathology, decreased survival | (95) |
| β2a-transgenic model (hyperactivation of L-type Ca2+ channel) | decreased pathology, increased survival | (150) |
| Carotid artery injury model | accelerated thrombosis | (151) |
| Renal IR | cytoprotection | (127, 128) |
| Acetaminophen hepatotoxicity | cytoprotection | (152) |
| Pdx1 haploinsufficient mice (heritable diabetes model) | preservation of pancreatic cells | (153) |
| Cerebral IR | decreased infarct size | (36, 126) |
| Cerebral Neonatal Hypoxia | increased injury | (126) |
| EAE (multiple sclerosis) | axon preservation (cytoprotection) | (154) |
| Amyloid-β mutant model (Alzheimer’s) | cytoprotection, improved learning and memory | (155, 156) |
| SOD1 G93A mutant model (ALS) | delayed disease onset, improved survival | (157) |
| Glutamate-excitotoxicity (ex vivo) | cytoprotection | (158) |
| MPTP neurotoxin administration (Parkinson’s) | acute model cytoprotective, chronic model no change | (159) |
| Sgcd−/− (muscular dystrophy) | reduced skeletal muscle pathology, cytoprotection | (143) |
| Lama2−/− (muscular dystrophy) | reduced pathology, increased survival | (143) |
| Col6a1−/− (muscular dystrophy) | reduced pathology, cytoprotection | (160) |
| Aging | adult-onset obesity | (114) |
| Aging | behavioral defects | (114) |
| Aging | decreased LV contractile reserve | (95) |
| Behavioral testing | impairments in memory | (161) |
| Endurance exercise (swimming) | increased hypertrophy and mortality | (95) |