Preclinical and clinical research on inflammation after intracerebral hemorrhage

By Jian Wang. Progress in neurobiology, 2010

595 citations recorded by the source corpus.

Intracerebral hemorrhage (ICH) is one of the most lethal stroke subtypes. Despite the high morbidity and mortality associated with ICH, its pathophysiology has not been investigated as well as that of ischemic stroke. Available evidence from preclinical and clinical studies suggests that inflammatory mechanisms are involved in the progression of ICH-induced secondary brain injury. For example, in preclinical ICH models, microglial activation has been shown to occur within 1 h, much earlier than neutrophil infiltration. Recent advances in our understanding of neuroinflammatory pathways have revealed several new molecular targets, and related therapeutic strategies have been tested in preclinical ICH models. This review summarizes recent progress made in preclinical models of ICH, surveys preclinical and clinical studies of inflammatory cells (leukocytes, macrophages, microglia, and astrocytes) and inflammatory mediators (matrix metalloproteinases, nuclear factor erythroid 2-related factor 2, heme oxygenase, and iron), and highlights the emerging areas of therapeutic promise.

Subfields: Epidemiology, Neurology

View Paper: https://www.semanticscholar.org/paper/fa2643455176b8a786ac85b899d9e7bc35654a3f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Qing-Wu Yang
2. Brent R. Stockwell

In Neurology

1. Qing-Wu Yang
2. Liang Liu
3. Brent R. Stockwell
4. Jian Wang
5. Xiao-Yi Xiong

Citations in the corpus

• Functions and mechanisms of microglia/macrophages in neuroinflammation and neurogenesis after stroke. (2016, background): “Both cell types express many of the same markers (e.g., CD11b, F4/80, Iba-1) (Ginhoux et al., 2010; Wang, 2010), which makes studies concerning microglial activity based on morphology difficult, and these cells are often overgeneralized as microglia/macrophages.”
• Inhibition of neuronal ferroptosis protects hemorrhagic brain. (2017, background): “Evidence from preclinical and clinical studies suggests that toxins released from an intracerebral hematoma may contribute to brain damage after ICH (2, 4–8).”
• Neuronal Cell Death. (2018, unknown): “In general, it is thought that the main mechanisms of neuronal death in hemorrhagic stroke are excitotoxicity, toxicity of blood, oxidative stress, and inflammation (19, 705).”