Roles of p38α mitogen‐activated protein kinase in mouse models of inflammatory diseases and cancer

Gupta, J. R. P.; Nebreda, Ángel R.

doi:10.1111/febs.13250

Cited by 126 publications

(110 citation statements)

References 122 publications

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“…P38MAPK and ERK1/2 may regulate oxidative stress and inflammatory responses [34, 35]. It is known that many I/R injury models elicited the activation of p38MAPK and ERK1/2 pathways [36–38].…”

Section: Discussionmentioning

confidence: 99%

Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-κB Pathways in Rats

Zhu

Cai

Zhou

et al. 2017

BioMed Research International

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Schisandrin B (ScB), isolated from Schisandra chinensis (S. chinensis), is a traditional Chinese medicine with proven cardioprotective and neuroprotective effects. However, it is unclear whether ScB also has beneficial effects on rat hind limb ischemia/reperfusion (I/R) injury model. In this study, ScB (20 mg/kg, 40 mg/kg, and 80 mg/kg) was administered via oral gavage once daily for 5 days before the surgery. After 6 h ischemia and 24 h reperfusion of left hind limb, ScB reduced I/R induced histological changes and edema. ScB also suppressed the oxidative stress through decreasing MDA level and increasing SOD activity. Moreover, above changes were associated with downregulated TNF-α mRNA expression and reduced level of IL-1β in plasma. Meanwhile, ScB treatment downregulated activation of p38MAPK, ERK1/2, and NF-κB in ischemic skeletal muscle. These results demonstrate that ScB treatment could prevent hind limb I/R skeletal muscle injury possibly by attenuating oxidative stress and inflammation via p38MAPK, ERK1/2, and NF-κB pathways.

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Section: Discussionmentioning

confidence: 99%

Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-κB Pathways in Rats

Zhu

Cai

Zhou

et al. 2017

BioMed Research International

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“…Additionally, the Western diet group did not significantly result in increased p38 activation as exhibited by the AIN-76A Mod, 6% SF, and 12% SF groups. The IL-6-STAT3 pathway has been shown to be a key regulator of colon cancer development (46), and it has recently been shown that p38 is required for cancer cell survival (20), and can serve as an activator of STAT3 (21). Thus, it is not surprising that the decreased p38 activity was associated with less STAT3 activation and proliferation in the Western diet group.…”

Section: Discussionmentioning

confidence: 99%

High-fat diets rich in saturated fat protect against azoxymethane/dextran sulfate sodium-induced colon cancer

Enos

Velázquez

McClellan

et al. 2016

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…2, 28 Since p38 MAPK plays a critical role in inducing inflammation in multiple tissue types, 19, 20, 32 we sought to evaluate whether inhibition of p38 MAPK could regulate the expression of several genes known to be regulated by p38 MAPK that are involved in inflammation in skeletal muscle tissue. IL1β and IL6 are potent proinflammatory cytokines known to direct atrophy and collagen production, 1, 12 and IL10 is an antiinflammatory gene that can protect against atrophy and fibrosis in skeletal muscle tissue.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of p38 mitogen-activated protein kinase signaling reduces fibrosis and lipid accumulation after rotator cuff repair

Wilde

Gumucio

Grekin

et al. 2016

Journal of Shoulder and Elbow Surgery

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Background The repair of rotator cuff tears is often complicated by fatty degeneration, which is the combination of lipid accumulation, fibrosis, inflammation and muscle weakness. p38 MAPK is a signaling molecule that plays a central role in these processes. The purpose of this study was to evaluate a small molecule inhibitor of p38 MAPK, SB203580, in reducing fatty degeneration in a preclinical model of rotator cuff injury and repair. Methods Adult rats underwent a bilateral supraspinatus tenotomy that was repaired 30 days later. Rats were treated with SB203580 or vehicle every 2 days with injections beginning 3 days prior to surgery, and continued until 7 days after surgery. Two weeks after surgical repair muscles were analyzed using histology, lipid profiling, gene expression and permeabilized muscle fiber contractility. Results Inhibition of p38 MAPK resulted in a nearly 49% reduction in fat accumulation and a 29% reduction in collagen content, along with changes in corresponding genes regulating adipogenesis and matrix accumulation. There was also a marked 40–80% decrease in the expression of several proinflammatory genes, including IL1β, IL6 and COX2, and a 360% increase in the antiinflammatory gene IL10. No differences were observed for muscle fiber force production. Conclusion Inhibition of p38 MAPK was found to have a significant decrease in intramuscular lipid accumulation and fibrosis that is usually seen in the degenerative cascade of rotator cuff tears, without having negative effects on the contractile properties of the rotator cuff muscle tissue.

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Roles of p38α mitogen‐activated protein kinase in mouse models of inflammatory diseases and cancer

Cited by 126 publications

References 122 publications

Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-κB Pathways in Rats

Schisandrin B Prevents Hind Limb from Ischemia-Reperfusion-Induced Oxidative Stress and Inflammation via MAPK/NF-κB Pathways in Rats

High-fat diets rich in saturated fat protect against azoxymethane/dextran sulfate sodium-induced colon cancer

Inhibition of p38 mitogen-activated protein kinase signaling reduces fibrosis and lipid accumulation after rotator cuff repair

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