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Agonistic analogs of growth hormone releasing hormone (GHRH) promote wound healing by stimulating the proliferation and survival of human dermal fibroblasts through ERK and AKT pathways.

evidence

This record provides bibliographic details and links to the original research. An editorial study breakdown is not available.

What the researchers found

The GHRH analogs MR-409 and MR-502 significantly increased proliferation of human dermal fibroblasts by over 50% in vitro and improved cell survival under stress. MR-409 applied topically in vivo accelerated wound closure in a dose-dependent manner and reduced fibrosis, acting through MEK/ERK and PI3K/AKT pathways independent of IGF-1 receptor signaling.

Why it matters

Finding agents that promote fibroblast growth and survival can improve wound healing outcomes. These GHRH analogs resist degradation and activate key cell survival pathways, making them promising candidates for therapeutic development.

How the study worked

The study used in vitro experiments with primary human dermal fibroblasts to assess proliferation and survival after treatment with GHRH analogs MR-409 and MR-502. In vivo wound healing was evaluated by topical application of MR-409 on animal models, with histological analysis of wound contraction and fibrosis.

What this study cannot tell us

The study does not specify the clinical trial phase or long-term safety data. The animal model results may not fully translate to humans without further testing.

Read the original research

Agonistic analogs of growth hormone releasing hormone (GHRH) promote wound healing by stimulating the proliferation and survival of human dermal fibroblasts through ERK and AKT pathways.

Oncotarget, 7(33), 52661-52672

Citation

Cui, Tengjiao; Jimenez, Joaquin J; Block, Norman L; Badiavas, Evangelos V; Rodriguez-Menocal, Luis; Vila Granda, Ailin; Cai, Renzhi; Sha, Wei; Zarandi, Marta; Perez, Roberto; Schally, Andrew V. (2016). Agonistic analogs of growth hormone releasing hormone (GHRH) promote wound healing by stimulating the proliferation and survival of human dermal fibroblasts through ERK and AKT pathways.. Oncotarget, 7(33), 52661-52672. https://doi.org/10.18632/oncotarget.11024