What does this research mean for the field?

The circ_ATP5A1/hsa-miR-145-5p/ZFP36 regulatory axis attenuates acute kidney injury by inhibiting ferroptosis and reducing inflammatory responses. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

Investigate whether circular RNA circ_ATP5A1 regulates ferroptosis and inflammation during acute kidney injury and delineate the underlying molecular mechanisms.

September 2, 2026HereditasOpen Access

circATP5A1 sponges hsa-miR-145-5p to regulate ZFP36 and ferroptosis-associated signaling in acute kidney injury

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Authors

PHPeng Huang LMLingzhang Meng JMJing Ma

Discussion

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Overview

Preclinical study reveals that circ_ATP5A1 suppresses ferroptosis and inflammation in acute kidney injury models, highlighting a novel therapeutic target for renal protection.

Key Points

Investigate whether circular RNA circ_ATP5A1 regulates ferroptosis and inflammation during acute kidney injury and delineate the underlying molecular mechanisms.
Constructed a circRNA-miRNA-mRNA network using bioinformatics and confirmed molecular interactions with dual-luciferase reporter and RNA immunoprecipitation assays.
Assessed cell viability, inflammatory cytokines, and ferroptosis markers in LPS-treated HK-2 tubular epithelial cells with circ_ATP5A1 overexpression.
Evaluated renal function and histopathological damage in an LPS-induced acute kidney injury mouse model with circ_ATP5A1 upregulation.
circ_ATP5A1 and ZFP36 were downregulated while hsa-miR-145-5p was upregulated in LPS-exposed HK-2 cells and AKI mice, with circ_ATP5A1 confirmed to act as a sponge for hsa-miR-145-5p to relieve repression of ZFP36.
circ_ATP5A1 overexpression enhanced HK-2 cell viability, reduced inflammatory cytokines (IL-1β, IL-6, TNF-α), elevated ferroptosis inhibitors GPX4 and SLC7A11, and diminished pro-ferroptotic ACSL4.
Upregulation of circ_ATP5A1 in vivo significantly attenuated renal dysfunction and structural tissue injury in LPS-challenged mice.

Cite This Study

Huang et al. (2026) studied this question.

synapsesocial.com/papers/6a97e25ec562ede874ec670a https://doi.org/10.1186/s41065-026-00734-2

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September 2, 2026HereditasOpen Access

circATP5A1 sponges hsa-miR-145-5p to regulate ZFP36 and ferroptosis-associated signaling in acute kidney injury

View Full Paper

Ask AI

Bookmark

Authors

PHPeng Huang LMLingzhang Meng JMJing Ma

Discussion

Member takes

Overview

Preclinical study reveals that circ_ATP5A1 suppresses ferroptosis and inflammation in acute kidney injury models, highlighting a novel therapeutic target for renal protection.

Key Points

Investigate whether circular RNA circ_ATP5A1 regulates ferroptosis and inflammation during acute kidney injury and delineate the underlying molecular mechanisms.
Constructed a circRNA-miRNA-mRNA network using bioinformatics and confirmed molecular interactions with dual-luciferase reporter and RNA immunoprecipitation assays.
Assessed cell viability, inflammatory cytokines, and ferroptosis markers in LPS-treated HK-2 tubular epithelial cells with circ_ATP5A1 overexpression.
Evaluated renal function and histopathological damage in an LPS-induced acute kidney injury mouse model with circ_ATP5A1 upregulation.
circ_ATP5A1 and ZFP36 were downregulated while hsa-miR-145-5p was upregulated in LPS-exposed HK-2 cells and AKI mice, with circ_ATP5A1 confirmed to act as a sponge for hsa-miR-145-5p to relieve repression of ZFP36.
circ_ATP5A1 overexpression enhanced HK-2 cell viability, reduced inflammatory cytokines (IL-1β, IL-6, TNF-α), elevated ferroptosis inhibitors GPX4 and SLC7A11, and diminished pro-ferroptotic ACSL4.
Upregulation of circ_ATP5A1 in vivo significantly attenuated renal dysfunction and structural tissue injury in LPS-challenged mice.

Cite This Study

Huang et al. (2026) studied this question.

synapsesocial.com/papers/6a97e25ec562ede874ec670a https://doi.org/10.1186/s41065-026-00734-2

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