Restoration of erectile function by a combination of antiapoptosis by JNK inhibitor and preservation of smooth muscle or endothelium by hepatocyte growth factor in a rat model of cavernous nerve injury.
Soo Woong KimJunghoon LeeSohee OhHwancheol SonMin Chul ChoPublished in: The Prostate (2021)
Our data indicated that the combined administration of a JNK inhibitor and medium or high-dose HGF to nerve-injured rats in the immediate post-injury period after CNCI may restore erectile function to a level comparable to the normal level by suppressing cavernosal apoptosis and preserving the integrity of SM or endothelium via rectification of the cJun and cMet/eNOS pathways.
Keyphrases
- growth factor
- smooth muscle
- high dose
- cell death
- nitric oxide
- signaling pathway
- induced apoptosis
- endoplasmic reticulum stress
- oxidative stress
- cell cycle arrest
- peripheral nerve
- low dose
- nitric oxide synthase
- electronic health record
- endothelial cells
- benign prostatic hyperplasia
- stem cell transplantation
- deep learning
- machine learning
- artificial intelligence