Will your incompetent doctor do nothing with this? Well, do you have an incompetent doctor, or not? No knowledge of ALL this earlier research would be my definition of incompetence!
Microglial Mechanisms and Therapeutic Potential in Brain Injury Post-Intracerebral Hemorrhage
Authors Gong Y, Li H, Cui H, Gong Y
Received 1 October 2024
Accepted for publication 13 February 2025
Published 26 February 2025 Volume 2025:18 Pages 2955—2973
DOI https://doi.org/10.2147/JIR.S498809
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Ning Quan
Yuhua Gong,1,2 Hui Li,1 Huanglin Cui,1 Yuping Gong2
1School
of Smart Health, Chongqing Polytechnic University of Electronic
Technology, Chongqing, 401331, People’s Republic of China; 2Ultrasound
Department of the Second Affiliated Hospital of Chongqing Medical
University, Chongqing, 400010, People’s Republic of China
Correspondence:
Yuhua Gong; Yuping Gong, Department of Ultrasound, the Second
Affiliated Hospital of Chongqing Medical University, Chongqing, 400010,
People’s Republic of China, Email gongyuhua@cqcet.edu.cn; gyp826@hospital.cqmu.edu.cn
Abstract:
Intracerebral hemorrhage (ICH) is a particularly common public health
problem with a high mortality and disability rate and no effective
treatments to enhance clinical prognosis. The increased aging
population, improved vascular prevention, and augmented use of
antithrombotic agents have collectively contributed to the rise in ICH
incidence over the past few decades. The exploration and understanding
of mechanisms and intervention strategies has great practical
significance for expanding treatments and improving prognosis of ICH.
Microglia, as resident macrophages of central nervous system, are
responsible for the first immune defense post-ICH. After ICH, M1
microglia is firstly activated by primary injury and thrombin;
subsequently, reactive microglia can further amplify the immune response
and exert secondary injury(Correctly called the
neuronal cascade of death! Signifying an immediate need to prevent that!
Neuroprotection is a milquetoast term saying nothing!)
(eg, oxidative stress, neuronal damage, and brain edema). The pro-inflammatory phenotype transmits to M2 microglia within 7 days post-ICH, which plays a key role in erythrophagocytosis and limiting the inflammatory secondary injury. Microglial M2 polarization has significant implications for improving prognosis, this process can be mediated through crosstalk with other cells, metabolic changes, and microbiota interaction. Clarifying the effect, timing, and potential downstream effects of multiple mechanisms that synergistically trigger anti-inflammatory responses may be necessary for clinical translation. Analyses of such intricate interaction between microglia cells and brain injury/repair mechanisms will contribute to our understanding of the critical microglial responses to microenvironment and facilitating the discovery of appropriate intervention strategies. Here, we present a comprehensive overview of the latest evidences on microglial dynamics following ICH, their role in driving primary/secondary injury mechanisms as well as neurorepair/plasticity, and possible treatment strategies targeting microglia.
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