Chronic neuropathic pain protect heart from ischemia reperfusion injury
Ischemic heart disease or coronary heart disease is the leading cause of death in the world and the 2nd cause of death in Taiwan. Timely restoration of blood flow is the most effective way to rescue myocardium. However, reperfusion can also damage cardiomyocytes due to calcium overload, free radical production and inflammatory cell infiltration. This phenomenon is called ischemia-reperfusion (IR) injury. A team led by Drs. Chien-Chang Chen and Bai Chuang Shyu at the Institute of Biomedical Sciences (IBMS) in Academia Sinica discovered a novel mechanism of chronic neuropathic pain induces cardioprotection against cardiac IR injury in mice. The research was published in the journal Nature Communications on October 10th, 2017.
Cardiac protection can be induced by ischemic preconditioning (IPC) or postconditioning in the heart. IPC can also be applied in distant tissues or organs to protect heart from IR injury which is called remote IPC. Prodromal angina, presented as a form of chest pain, can limit infarct size and is speculated as an innate cardioprotection. Although preinfarction angina-associated cardioprotection is thought to represent a clinical correlation of IPC, it is possible that angina also induces nociceptive signal pathway to provide cardioprotection. It is unclear whether pre-existing chronic pain will also have a similar cardioprotective effect.
Up to 25% of the population is suffering from chronic pain, especially in elder. Ischemic heart disease is also prevalent in the elderly population. However, it is unclear whether this is a relationship between chronic pain and ischemic heart diseases. The team discovered that chronic neuropathic pain in mice reduced IR injury. They showed that the ERK activity and neuronal activity in the anterior nucleus of the paraventricular thalamus (PVA), is required for the chronic neuropathic pain-induced cardioprotection. In addition, direct activation of PVA neuron using pharmacological or optogenetic tools without peripheral injury also provided cardioprotection. Inhibition of parasympathetic nerve activity abolished chronic neuropathic pain-induced cardioprotection. Overall, the team demonstrates that chronic pain induces cardioprotection via a novel central mechanism involving activation of PVA neurons.
The article entitled “Cardioprotection induced in a mouse model of neuropathic pain via anterior nucleus of paraventricular thalamus” can be found at: https://www.nature.com/articles/s41467-017-00891-z
The complete list of authors is: Yi-Fen Cheng, Ya-Ting Chang, Wei-Hsin Chen, Hsi-Chien Shih, Yen-Hui Chen, Bai-Chuang Shyu and Chien-Chang Chen
Media contact:
Dr. Chien-Chang Chen, Institute of Biomedical Sciences, Academia Sinica
Email: ccchen@ibms.sinica.edu.tw; (Tel) +886-2-2652-3522