Cited by 276Neuroinflammation and Neurodegeneration MechanismsAcute Ischemic Stroke ManagementTryptophan and brain disorders

Systemic inflammation after stroke: implications for post‐stroke comorbidities

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Simats, Alba, Liesz, Arthur·2022·EMBO Molecular Medicine

Abstract

Immunological mechanisms have come into the focus of current translational stroke research, and the modulation of neuroinflammatory pathways has been identified as a promising therapeutic approach to protect the ischemic brain. However, stroke not only induces a local neuroinflammatory response but also has a profound impact on systemic immunity. In this review, we will summarize the consequences of ischemic stroke on systemic immunity at all stages of the disease, from onset to long-term outcome, and discuss underlying mechanisms of systemic brain-immune communication. Furthermore, since stroke commonly occurs in patients with multiple comorbidities, we will also overview the current understanding of the potential role of systemic immunity in common stroke-related comorbidities, such as cardiac dysfunction, atherosclerosis, diabetes, and infections. Finally, we will highlight how targeting systemic immunity after stroke could improve long-term outcomes and alleviate comorbidities of stroke patients.

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Crossref · 10.15252/emmm.202216269

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  • Excessive or dysregulated inflammation is a major driver of tissue damage and the pathogenesis of numerous diseases, including stroke, Parkinson's disease, atherosclerosis, and cancer.

    “Excessive or dysregulated inflammation is a major driver of tissue damage and the pathogenesis of numerous diseases, including stroke, Parkinson’s disease, atherosclerosis, and cancer [9,30,31,32,33].”

    From Picroside II as a Potential Anti-Inflammatory Agent (2026) · cites this paper as [32]

    The Acute systemic inflammatory response section says inflammatory cytokines contribute to blood–brain barrier breakdown and are associated with larger infarcts after stroke. The Atherosclerosis section describes inflammatory mechanisms throughout plaque formation. Our copy does not address Parkinson’s disease or cancer in this connection, so it supports only part of the disease list attributed to this source (no page numbers are available). (LLM, conf=0.87)

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Cited by

Sorted by citations

Authors
Simats, A., & Liesz, A.
Affiliations
LMU Klinikum (DE)
Corresponding author
Liesz, Arthur
Venue
EMBO Molecular Medicine
Published
2022-08-15
Volume
14
Issue
9
Pages
e16269-e16269
ISSN
  • 1757-4676 (ISSN-L)
  • 1757-4684
OpenAlex
W4292178757
Cited by
276
References
12
Citations by year
2026: 76 · 2025: 87 · 2024: 68 · 2023: 40 · 2022: 5
FWCI
5.18
Type
journal article
Language
en
Open access
Locations
  • EMBO Molecular Medicine (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Open access LMU (Ludwid Maxmilian's Universitat Munchen) (submittedVersion, cc-by)
Funders
  • Deutsche Forschungsgemeinschaft (EXC 2145 SyNergy ‐ ID 390857198, FOR 2879 (LI‐2534/5‐1), SI 2832/1‐1)
  • EC ¦ ERC ¦ HORIZON EUROPE European Research Council (ERC‐StGs 802305)
  • Stiftung zur Erforschung der Vaskulären Demenz
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
systemic inflammation, ischemic stroke, systemic immunity, neuroinflammation, brain-immune communication, stroke comorbidities, cardiac dysfunction, atherosclerosis, diabetes mellitus, post-stroke infection, immunomodulation
MeSH terms
Brain, Brain Ischemia, Humans, Inflammation, Stroke, Translational Research, Biomedical

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