ReviewFrontiers in psychiatry2018
Mechanisms and Therapeutic Targets of Depression After Intracerebral Hemorrhage.
Review in Frontiers in psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Associations between composite dietary antioxidant index and depressive symptoms among pregnant and postpartum women.BMC pregnancy and childbirth · 2026Article
- SPP1/OPN Alleviates Post-Intracerebral Hemorrhage Depression and Cognitive Impairment via Nrf2/BDNF Signaling Activation in Mice.CNS neuroscience & therapeutics · 2025Article
- Emerging Therapeutic Strategies in Intracerebral Hemorrhage: Enhancing Neurogenesis and Functional Recovery.MedComm · 2025Review
- Diagnosis and etiology of poststroke depression: A review.World journal of psychiatry · 2025Review
- Luteolin and triptolide: Potential therapeutic compounds for post-stroke depression via protein STAT.Heliyon · 2023Article
- Depression in Patients With Intracranial Hemorrhage Secondary to Traumatic Brain Injury.Cureus · 2023Article
- Elevated red blood cell distribution width levels predict depression after intracerebral hemorrhage: A 3-month follow-up study.Frontiers in neurology · 2023Article
- Amelioration of Brain Damage after Treatment with the Methanolic Extract ofPharmaceutics · 2022Article
- Glycosaminoglycan scaffolding and neural progenitor cell transplantation promotes regenerative immunomodulation in the mouse ischemic brain.Experimental neurology · 2022Article
- Zein-Stabilized Nanospheres as Nanocarriers for Boosting the Aphrodisiac Activity of Icariin: Response Surface Optimization and In Vivo Assessment.Pharmaceutics · 2022Article
- Neuroprotective Effect of Chrysophanol as a PI3K/AKT/mTOR Signaling Inhibitor in an Experimental Model of Autologous Blood-induced Intracerebral Hemorrhage.Current medical science · 2022Article
- Neuroprotective Effect of Chrysophanol as a PI3K/AKT/mTOR Signaling Inhibitor in an Experimental Model of Autologous Blood-induced Intracerebral Hemorrhage.Current medical science · 2022Article
- Diet-Induced High Serum Levels of Trimethylamine-N-oxide Enhance the Cellular Inflammatory Response without Exacerbating Acute Intracerebral Hemorrhage Injury in Mice.Oxidative medicine and cellular longevity · 2022Article
- Targeting C-C Chemokine Receptor 5: Key to Opening the Neurorehabilitation Window After Ischemic Stroke.Frontiers in cellular neuroscience · 2022Review
- Orexin-A exerts neuroprotective effect in experimental intracerebral hemorrhage by suppressing autophagyFrontiers in cellular neuroscience · 2022Article
- Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?Frontiers in cellular neuroscience · 2022Review
- Expression and role of microRNA-212/nuclear factor I-A in depressive mice.Bioengineered · 2021Article
- The molecular mechanism underlying mitophagy-mediated hippocampal neuron apoptosis in diabetes-related depression.Journal of cellular and molecular medicine · 2021Article
- CCR5-Δ32 polymorphism: a possible protective factor for post-stroke depressive symptoms.Journal of psychiatry & neuroscience : JPN · 2021Article
- Neurovascular Units and Neural-Glia Networks in Intracerebral Hemorrhage: from Mechanisms to Translation.Translational stroke research · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The relationship between depression and intracerebral hemorrhage (ICH) is complicated. One of the most common neuropsychiatric comorbidities of hemorrhagic stroke is Post-ICH depression. Depression, as a neuropsychiatric symptom, also negatively impacts the outcome of ICH by enhancing morbidity, disability, and mortality. However, the ICH outcome can be improved by antidepressants such as the frequently-used selective serotonin reuptake inhibitors. This review therefore presents the mechanisms of post-ICH depression, we grouped the mechanisms according to inflammation, oxidative stress (OS), apoptosis and autophagy, and explained them through their several associated signaling pathways. Inflammation is mainly related to Toll-like receptors (TLRs), the NF-kB mediated signal pathway, the PPAR-γ-dependent pathway, as well as other signaling pathways. OS is associated to nuclear factor erythroid-2 related factor 2 (Nrf2), the PI3K/Akt pathway and the MAPK/P38 pathway. Moreover, autophagy is associated with the mTOR signaling cascade and the NF-kB mediated signal pathway, while apoptosis is correlated with the death receptor-mediated apoptosis pathway, mitochondrial apoptosis pathway, caspase-independent pathways and others. Furthermore, we found that neuroinflammation, oxidative stress, autophagy, and apoptosis experience interactions with one another. Additionally, it may provide several potential therapeutic targets for patients that might suffer from depression after ICH.
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