Inflammatory responses involved in post-cardiac arrest brain injury: mechanisms, regulation, and therapeutic potential

Author:

Zhang Yuzhen1,Li Zhentong1,Zhang Kunxue1,Chang Yuan1,Chen Jiancong1,Al-Nusaif Murad2,Pan Suyue1ORCID,Huang Kaibin1ORCID

Affiliation:

1. Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong, China

2. Neurology Department and Liaoning Provincial Key Laboratory for Research on the Pathogenic Mechanisms of Neurological Diseases, First Affiliated Hospital, Dalian Medical University, Dalian 116014, Liaoning, China

Abstract

Neuroinflammation plays a key role in the pathogenesis of post-cardiac arrest (CA) brain injury. Innate immune cells sense a variety of danger signals through pattern-recognition receptors and evoke rapidly after ischemic challenge, triggering inflammatory responses and amplifying brain damage. A programmed cell death (PCD) pathway is activated after ischemic and/or inflammatory stimuli, leading to the elimination of the damaged cells. However, PCD also regulates inflammatory responses flexibly. The present review aimed to summarize the mechanisms of inflammatory responses, including the biology of immune cells, the innate immune recognition that initiates the inflammation, and the immunomodulatory effects of PCD following CA. Promising therapeutic approaches of targeting inflammatory responses to alleviate brain injury and improve neurological outcomes after CA are also reviewed.

Funder

National Natural Science Foundation of China

Basic and Applied Basic Research Foundation of Guangdong Province

Publisher

Open Exploration Publishing

Subject

General Medicine,General Earth and Planetary Sciences,General Environmental Science,Psychiatry and Mental health,Pharmacology (medical),General Medicine,General Medicine,General Medicine,General Engineering,General Medicine,Management of Technology and Innovation

Reference118 articles.

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