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Histopathological and ultrastructural changes in different cell types during ischemic and hemorrhagic stroke
Introduction
Stroke continues to represent the second leading cause of death globally (Feigin, Brainin et al. 2022). Despite an 18.2% decline in incidence among individuals aged 70 years and older from 1990 to 2021, indicating a potential shift toward younger onset, the elderly demographic remains predominant in stroke epidemiology, with prevalence for those aged 70 and above being nearly ten times higher than in younger populations (Collaborators 2024). Projections indicate that the global death toll from stroke could rise by 50% by 2050, escalating from 6.6 million in 2020 to 9.7 million (Feigin and Owolabi 2023). Furthermore, the estimated global economic burden of stroke surpasses US$721 billion, accounting for approximately 0.66% of worldwide GDP (Feigin, Brainin et al. 2022). This staggering economic burden underscores the urgent need for more research and policy changes.
Ischemic stroke, primarily resulting from the blockage of cerebral arteries due to blood clots, constitutes about 65.3% (62.4–67.7) of cases. In contrast, intracerebral hemorrhage (ICH), which involves the rupture of a small brain artery leading to blood leakage into the brain parenchyma, represents 28.8% (28.3–28.8) of cases. Lastly, subarachnoid hemorrhage (SAH) accounts for 5.8% of incident strokes (Collaborators 2024).
In recent years, stroke research has directed considerable attention towards key pathophysiologic mechanisms, such as excitotoxicity (Tuo et al., 2022, Li et al., 2023), neuroinflammation (Wang, Wang et al. 2024), mitochondrial dysfunction (Jia et al., 2021, Li et al., 2022), cell death (Datta et al., 2020, Gou et al., 2021), and blood-brain barrier (BBB) impairment (Luo et al., 2019, Meijer and Gorter, 2024). While these investigations have profoundly advanced our understanding of the mechanisms underlying stroke at both molecular and cellular levels, exploring dynamic ultrastructural changes associated with these processes remains insufficiently addressed. The connection between ultrastructural changes and pathophysiological studies is notably robust. For instance, mitochondrial fragmentation and dysfunction at the ultrastructural level serve as direct reflections of functional deficits in energy metabolism and neuronal communication, which are key manifestations of redox imbalance following cerebral ischemia (Li et al., 2022, Hossain et al., 2024). Transmission electron microscopy (TEM) provides invaluable insights into these alterations by enabling the visualization of organelles and revealing critical indicators of cellular injury, such as mitochondrial swelling, mitochondrial condensation, endoplasmic reticulum stress, and nuclear alterations (Zille, Farr et al. 2012). Additionally, TEM facilitates differentiated regulated cell death types based on their distinct morphological characteristics (Zille, Farr et al. 2012).
Current studies on ultrastructural changes after stroke have predominantly concentrated on a specific stroke subtype. This review aims to comprehensively analyze and summarize the ultrastructural alterations observed in neurons, synapses, glial cells, and the BBB following ischemic stroke, ICH, and SAH. To our knowledge, this represents the first thorough overview of the dynamic subcellular structure changes targeting the significant components of brain cells across three preclinical stroke models. Such analysis is expected to significantly enhance our understanding of the complex pathological cascade that follows stroke and provide a holistic perspective to inform and inspire future diagnostic and therapeutic endeavors.
We conducted a literature search on PubMed, focusing on the ultrastructural changes in the brain observed through TEM following stroke, highlighting the associated mechanisms and pathological processes identified in preclinical studies. The keywords used in our search included “ischemic stroke,” “hemorrhagic stroke,” “intracerebral hemorrhage,” “cerebral hemorrhage,” “cerebral ischemia,” “subarachnoid hemorrhage,” “middle cerebral artery occlusion,” “ultrastructural changes,” “transmission electron microscopy,” “ICH,” “SAH,” and “MCAO”. We searched for these terms across titles, abstracts, and full-text documents.
Publications were included based on the following criteria: (1) Studies conducted on animal models; (2) Reports detailing histopathological changes in the brain; (3) Research focusing on disease models of cerebral hemorrhage or cerebral ischemia; and (4) Publications written in English. Three independent researchers carried out the article selection process to ensure accuracy and minimize errors in material retrieval.
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