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Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review

The immense neuroinflammation induced by multiple sclerosis (MS) promotes a favorable environment for ischemic stroke (IS) development, making IS a deadly complication of MS. The overlapping inflammation in MS and IS is a prelude to the vascular pathology, and an inherent cell death mechanism that e...

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Autores principales: Monsour, Molly, Gordon, Jonah, Lockard, Gavin, Borlongan, Cesar V.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10387781/
https://www.ncbi.nlm.nih.gov/pubmed/37515536
http://dx.doi.org/10.1177/09636897231184596
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author Monsour, Molly
Gordon, Jonah
Lockard, Gavin
Borlongan, Cesar V.
author_facet Monsour, Molly
Gordon, Jonah
Lockard, Gavin
Borlongan, Cesar V.
author_sort Monsour, Molly
collection PubMed
description The immense neuroinflammation induced by multiple sclerosis (MS) promotes a favorable environment for ischemic stroke (IS) development, making IS a deadly complication of MS. The overlapping inflammation in MS and IS is a prelude to the vascular pathology, and an inherent cell death mechanism that exacerbates neurovascular unit (NVU) impairment in the disease progression. Despite this consequence, no therapies focus on reducing IS incidence in patients with MS. To this end, the preclinical and clinical evidence we review here argues for cell-based regenerative medicine that will augment the NVU dysfunction and inflammation to ameliorate IS risk.
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spelling pubmed-103877812023-08-01 Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review Monsour, Molly Gordon, Jonah Lockard, Gavin Borlongan, Cesar V. Cell Transplant Review The immense neuroinflammation induced by multiple sclerosis (MS) promotes a favorable environment for ischemic stroke (IS) development, making IS a deadly complication of MS. The overlapping inflammation in MS and IS is a prelude to the vascular pathology, and an inherent cell death mechanism that exacerbates neurovascular unit (NVU) impairment in the disease progression. Despite this consequence, no therapies focus on reducing IS incidence in patients with MS. To this end, the preclinical and clinical evidence we review here argues for cell-based regenerative medicine that will augment the NVU dysfunction and inflammation to ameliorate IS risk. SAGE Publications 2023-07-29 /pmc/articles/PMC10387781/ /pubmed/37515536 http://dx.doi.org/10.1177/09636897231184596 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Review
Monsour, Molly
Gordon, Jonah
Lockard, Gavin
Borlongan, Cesar V.
Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review
title Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review
title_full Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review
title_fullStr Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review
title_full_unstemmed Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review
title_short Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review
title_sort stem cells attenuate the inflammation crosstalk between ischemic stroke and multiple sclerosis: a review
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10387781/
https://www.ncbi.nlm.nih.gov/pubmed/37515536
http://dx.doi.org/10.1177/09636897231184596
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