ArticleMolecular medicine reports2021
Study of the pathology and the underlying molecular mechanism of tissue injury around hematoma following intracerebral hemorrhage.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 14 citations in OpenAlex.
- U shaped relationship between serum glucose potassium ratio and mortality in critically ill patients with toxic encephalopathy.Scientific reports · 2025Article
- Dynamic changes in chromatin accessibility within one month of mouse intracerebral hemorrhage.iScience · 2025Article
- Identification of stroke biomarkers using proteomic profiling of extracellular vesicles derived from human blood: a preliminary study.Frontiers in neurology · 2025Article
- Knowledge, attitudes, and practices regarding the prevention of intracerebral hemorrhage among hypertensive patients.Frontiers in cardiovascular medicine · 2025Article
- Ubiquitin-like 4A alleviates the progression of intracerebral hemorrhage by regulating oxidative stress and mitochondrial damage.Experimental animals · 2024Article
- FERM domain containing kindlin 1 knockdown attenuates inflammation induced by intracerebral hemorrhage in rats via NLR family pyrin domain containing 3/nuclear factor kappa B pathway.Experimental animals · 2023Article
- p75Neurotoxicity research · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracerebral hemorrhage (ICH) refers to hemorrhage caused by spontaneous rupture of blood vessels in the brain. Brain injury due to ICH leads to catastrophic effects resulting from the formation of hematoma and oxidative stress caused by components of lysed erythrocytes. However, not all neurons in the area surrounding the hematoma die immediately: A number of neurons remain in a critical, but reversible, state; however, the genes involved in this critical state remain poorly understood. Gene chip technology was used identify changes in the area surrounding the hematoma associated with the upregulation of 210 and downregulation of 173 genes. Gene Ontology functional annotation revealed changes in the gene expression profile in the peripheral region of hematoma following ICH, which were primarily associated with the external stimulation received by the organism, the transmission of harmful information to the cell through the transport of cell membrane proteins, and the regulation of a series of biological processes. Protein interaction network analysis revealed that 11 up‑[secreted phosphoprotein 1, dual specificity phosphatase 9, catechol‑O‑methyltransferase, BAR/IMD domain‑containing adaptor protein 2‑like 1, plakophilin 2, homer scaffold protein 3, ret proto‑oncogene (RET), KIT proto‑oncogene, receptor tyrosine kinase, hepsin, connector enhancer of kinase suppressor of Ras 2 and kalirin RhoGEF kinase] and four downregulated genes (transcription factor AP‑2β, peptidylprolyl isomerase A, SHOC2 leucine rich repeat scaffold protein and synuclein α) may serve a significant role in the area around hematoma following ICH. Reverse transcription‑quantitative PCR was used to verify that these genes were differentially expressed in the ICH compared with the control group. Causal network analysis suggested that the Achaete‑scute homolog 1‑RET signaling axis served a key role in the repair of nerve injury in the peripheral region of hematoma following ICH. Additionally,
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