IMR Press / FBL / Volume 27 / Issue 1 / DOI: 10.31083/j.fbl2701031
Open Access Systematic Review
Isoform-specific and cell/tissue-dependent effects of p38 MAPKs in regulating inflammation and inflammation-associated oncogenesis
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1 Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53223, USA
2 Research Service, Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, WI 53295, USA

Academic Editor: Graham Pawelec

Front. Biosci. (Landmark Ed) 2022, 27(1), 31;
Submitted: 11 November 2021 | Revised: 29 December 2021 | Accepted: 29 December 2021 | Published: 18 January 2022
Copyright: © 2022 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

p38 MAPK (mitogen-activated protein kinases) family proteins (α, β, γ and δ) are key inflammatory kinases and play an important role in relaying and processing intrinsic and extrinsic signals in response to inflammation, stress, and oncogene to regulate cell growth, cell death and cell transformation. Recent studies in genetic mouse models revealed that p38α in epithelial cells mostly suppresses whereas in immune cells it promotes inflammation and inflammation-associated oncogenesis. On the contrary, p38γ and p38δ signaling in immune and epithelial cells is both pro-inflammatory and oncogenic. This review summarizes recent discoveries in this field, discusses possible associated mechanisms, and highlights potentials of systemically targeting isoform-specific p38 MAPKs. Understanding of p38 MAPK isoform-specific and cell/tissue- and perhaps stage-dependent effects and their integrated regulated activity in inflammation and in inflammation-associated oncogenesis is essential for effectively targeting this group of kinases for therapeutic intervention.

p38 MAPKs
Isoform-specific and cell/tissue-dependent effects
Inflammation-associated oncogenesis
Fig. 1.
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