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Growth factor therapy sequesters inflammation in affording neuroprotection in cerebrovascular diseases.

ABSTRACT: In recent years, accumulating evidence has demonstrated the key role of inflammation in the progression of cerebrovascular diseases. Inflammation can persist over prolonged period of time after the initial insult providing a wider therapeutic window. Despite the acute endogenous upregulation of many growth factors after the injury, it is not sufficient to protect against inflammation and to regenerate the brain. Therapeutic approaches targeting both dampening inflammation and enhancing growth factors are likely to provide beneficial outcomes in cerebrovascular disease.In this mini review, we discuss major growth factors and their beneficial properties to combat the inflammation in cerebrovascular diseases. Emerging biotechnologies which facilitate the therapeutic effects of growth factors are also presented in an effort to provide insights into the future combination therapies incorporating both central and peripheral abrogation of inflammation. Expert commentary: Many studies discussed in this review have demonstrated the therapeutic effects of growth factors in treating cerebrovascular diseases. It is unlikely that one growth factor can be used to treat these complex diseases. Combination of growth factors and anti-inflammatory modulators may clinically improve outcomes for patients. In particular, transplantation of stem cells may be able to achieve both goals of modulating inflammation and upregulating growth factors. Large preclinical studies and multiple laboratory collaborations are needed to advance these findings from bench to bedside.

SUBMITTER: Nguyen H

PROVIDER: S-EPMC5057178 | biostudies-other | 2016 Aug

REPOSITORIES: biostudies-other

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Growth factor therapy sequesters inflammation in affording neuroprotection in cerebrovascular diseases.

Nguyen Hung H Aum David D Mashkouri Sherwin S Rao Gautam G Vega Gonzales-Portillo Juan Diego JD Reyes Stephanny S Borlongan Cesario V CV

Expert review of neurotherapeutics 20160513 8

<h4>Introduction</h4>In recent years, accumulating evidence has demonstrated the key role of inflammation in the progression of cerebrovascular diseases. Inflammation can persist over prolonged period of time after the initial insult providing a wider therapeutic window. Despite the acute endogenous upregulation of many growth factors after the injury, it is not sufficient to protect against inflammation and to regenerate the brain. Therapeutic approaches targeting both dampening inflammation an ...[more]

PMID: 27152762

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Project description:IMPORTANCE:Traumatic brain injury (TBI) is a significant public health concern that affects individuals in all demographics. With increasing interest in the medical and public communities, understanding the inflammatory mechanisms that drive the pathologic and consequent cognitive outcomes can inform future research and clinical decisions for patients with TBI. OBJECTIVES:To review known inflammatory mechanisms in TBI and to highlight clinical trials and neuroprotective therapeutic manipulations of pathologic and inflammatory mechanisms of TBI. EVIDENCE REVIEW:We searched articles in PubMed published between 1960 and August 1, 2014, using the following keywords: traumatic brain injury, sterile injury, inflammation, astrocytes, microglia, monocytes, macrophages, neutrophils, T cells, reactive oxygen species, alarmins, danger-associated molecular patterns, purinergic receptors, neuroprotection, and clinical trials. Previous clinical trials or therapeutic studies that involved manipulation of the discussed mechanisms were considered for inclusion. The final list of selected studies was assembled based on novelty and direct relevance to the primary focus of this review. FINDINGS:Traumatic brain injury is a diverse group of sterile injuries induced by primary and secondary mechanisms that give rise to cell death, inflammation, and neurologic dysfunction in patients of all demographics. Pathogenesis is driven by complex, interacting mechanisms that include reactive oxygen species, ion channel and gap junction signaling, purinergic receptor signaling, excitotoxic neurotransmitter signaling, perturbations in calcium homeostasis, and damage-associated molecular pattern molecules, among others. Central nervous system resident and peripherally derived inflammatory cells respond to TBI and can provide neuroprotection or participate in maladaptive secondary injury reactions. The exact contribution of inflammatory cells to a TBI lesion is dictated by their anatomical positioning as well as the local cues to which they are exposed. CONCLUSIONS AND RELEVANCE:The mechanisms that drive TBI lesion development as well as those that promote repair are exceedingly complex and often superimposed. Because pathogenic mechanisms can diversify over time or even differ based on the injury type, it is important that neuroprotective therapeutics be developed and administered with these variables in mind. Due to its complexity, TBI has proven particularly challenging to treat; however, a number of promising therapeutic approaches are now under pre-clinical development, and recent clinical trials have even yielded a few successes. Given the worldwide impact of TBI on the human population, it is imperative that research remains active in this area and that we continue to develop therapeutics to improve outcome in afflicted patients.

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Growth factor therapy sequesters inflammation in affording neuroprotection in cerebrovascular diseases.

Publications

Growth factor therapy sequesters inflammation in affording neuroprotection in cerebrovascular diseases.

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