What does this research mean for the field?

SIRT1 exerts protective effects in pediatric functional dyspepsia by deacetylating DRP1 at lysine 283, which inhibits excessive mitophagy and ameliorates mitochondrial dysfunction and oxidative stress. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This study investigates the role of SIRT1 in mitochondrial quality control and its therapeutic implications for pediatric functional dyspepsia.

May 10, 2026BMC ImmunologyOpen Access

SIRT1-mediated deacetylation of DRP1 suppresses excessive mitophagy and ameliorates pediatric functional dyspepsia

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Authors

SYShuan Yin DDDongdong Dai GWGaoyan Wang

Discussion

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Overview

Randomized trial investigates SIRT1's role in mitochondrial function in pediatric functional dyspepsia, suggesting therapeutic potential.

Key Points

This study investigates the role of SIRT1 in mitochondrial quality control and its therapeutic implications for pediatric functional dyspepsia.
Analyzed serum samples from pediatric functional dyspepsia patients and controls for SIRT1 and cytokines.
Human gastric smooth muscle cells were treated with CCCP to induce stress and assess mitochondrial function and mitophagy.
Utilized qPCR, Western blot, and functional assays to evaluate oxidative stress markers and protein interactions.
SIRT1 was significantly downregulated in both patient sera and CCCP-stimulated cells with increased pro-inflammatory cytokines (IL-6, TNF-α, IL-1β).
SIRT1 overexpression improved mitochondrial functions and inhibited excessive mitophagy and oxidative stress.
Deacetylation of DRP1 by SIRT1 was confirmed, leading to reduced mitophagy and oxidative stress in treated cells.

Cite This Study

Yin et al. (2026) studied this question.

synapsesocial.com/papers/6a0021e6c8f74e3340f9cccf https://doi.org/10.1186/s12865-026-00842-8

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May 10, 2026BMC ImmunologyOpen Access

SIRT1-mediated deacetylation of DRP1 suppresses excessive mitophagy and ameliorates pediatric functional dyspepsia

View Full Paper

Ask AI

Bookmark

Authors

SYShuan Yin DDDongdong Dai GWGaoyan Wang

Discussion

Member takes

Overview

Randomized trial investigates SIRT1's role in mitochondrial function in pediatric functional dyspepsia, suggesting therapeutic potential.

Key Points

This study investigates the role of SIRT1 in mitochondrial quality control and its therapeutic implications for pediatric functional dyspepsia.
Analyzed serum samples from pediatric functional dyspepsia patients and controls for SIRT1 and cytokines.
Human gastric smooth muscle cells were treated with CCCP to induce stress and assess mitochondrial function and mitophagy.
Utilized qPCR, Western blot, and functional assays to evaluate oxidative stress markers and protein interactions.
SIRT1 was significantly downregulated in both patient sera and CCCP-stimulated cells with increased pro-inflammatory cytokines (IL-6, TNF-α, IL-1β).
SIRT1 overexpression improved mitochondrial functions and inhibited excessive mitophagy and oxidative stress.
Deacetylation of DRP1 by SIRT1 was confirmed, leading to reduced mitophagy and oxidative stress in treated cells.

Cite This Study

Yin et al. (2026) studied this question.

synapsesocial.com/papers/6a0021e6c8f74e3340f9cccf https://doi.org/10.1186/s12865-026-00842-8

View Full Paper

Ask AI

Bookmark