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P38 MAPK linked to epigenetic activation of fibrotic genes in senescent lung fibroblasts

A new study reveals that p38 MAPK plays a key role in epigenetic regulation of fibrotic genes in lung fibroblasts, particularly in senescent cells. Pharmacological inhibition of p38 MAPK significantly reduced α-SMA and Col3A1 expression, suggesting a potential therapeutic target for treating age-related fibrotic diseases like IPF.

SourceImpact Journals LLC·JournalAging-US·TypeNews article·DateMar 10, 2026

Development of new p38 protein inhibitors with therapeutic potential for some heart diseases

Researchers at IRB Barcelona have developed new p38 inhibitors that selectively impair one of the activation pathways of the protein, allowing it to perform many of its normal functions. The inhibitors show therapeutic potential for heart diseases such as cardiac cell death and cardiotoxicity.

SourceInstitute for Research in Biomedicine (IRB Barcelona)·JournalNature Communications·TypeExperimental study·DateJul 13, 2023

Control hub for skin inflammation discovered

Researchers at the University of Bonn have identified a new signaling pathway that triggers inflammatory responses in the skin after UV damage. This pathway involves the activation of p38 molecularly modifying NLRP1, a critical switch for inflammation, and initiates the assembly of inflammasomes.

SourceUniversity of Bonn·JournalJournal of Experimental Medicine·DateNov 2, 2022

CNIC scientists uncover opposing roles of p38 proteins in cardiac hypertrophy

A study by CNIC scientists has identified a key role for the MKK3/6–p38γ/δ signaling pathway in cardiac hypertrophy. Inhibition of p38α promotes an unexpected activation of the other branch of the pathway, consisting of the proteins MKK3, p38γ, and p38δ. This activation induces another key pathway in cardiac hypertrophy, the mTOR pathway.

To die or not to die in response to stress, a decision regulated by MK2 protein levels

The study reveals that MK2 protein levels act as a molecular indicator for cell survival or death, with higher levels associated with cell death and lower levels linked to survival. Moderate stress triggers temporary activation of the p38-MK2 pathway, allowing cells to recover.

SourceInstitute for Research in Biomedicine (IRB Barcelona)·JournalProceedings of the National Academy of Sciences·DateJul 19, 2021