Cellular signallingApr 7, 2024

Long Noncoding RNA HMOX1 may reduce kidney damage caused by blood flow loss and return through the miR-3587/HMOX1 pathway

Updated Feb 20, 2026

Abstract

The expression of lnc-HMOX1 was reduced in renal tubular epithelial cells subjected to hypoxia-reoxygenation.

Long non-coding RNA heme oxygenase 1 (lnc-HMOX1) may have a biological function in renal ischemia reperfusion (RIR) injury.
Over-expression of lnc-HMOX1 could mitigate ferroptotic injury in renal tubular epithelial cells both in vivo and in vitro.
lnc-HMOX1 may function as a competitive endogenous RNA, promoting HMOX1 expression by sponging miR-3587.
Inhibition of HMOX1 appears to impede the protective effects of lnc-HMOX1 against ferroptotic injury.
Manipulating miR-3587 could reverse the effects of lnc-HMOX1 on ferroptotic injury during hypoxia-reoxygenation.

Simplified

Emerging evidence suggests that long non-coding RNAs (lncRNAs) play significant roles in renal ischemia reperfusion (RIR) injury. However, the specific mechanisms by which lncRNAs regulate ferroptosis in renal tubular epithelial cells remain largely unknown. The objective of this study was to investigate the biological function of lncRNA heme oxygenase 1 (lnc-HMOX1) in RIR and its potential molecular mechanism. Our findings demonstrated that the expression of HMOX1-related lnc-HMOX1 was reduced in renal tubular epithelial cells treated with hypoxia-reoxygenation (HR). Furthermore, the over-expression of lnc-HMOX1 mitigated ferroptotic injury in renal tubular epithelial cells in vivo and in vitro. Mechanistically, lnc-HMOX1, as a competitive endogenous RNA (ceRNA), promoted the expression of HMOX1 by sponging miR-3587. Furthermore, the inhibition of HMOX1 effectively impeded the aforementioned effects exerted by lnc-HMOX1. Ultimately, the inhibitory or mimic action of miR-3587 reversed the promoting or refraining influence of silenced or over-expressed lnc-HMOX1 on ferroptotic injury during HR. In summary, our findings contribute to a comprehensive comprehension of the mechanism underlying ferroptotic injury mediated by lnc-HMOX1 during RIR. Significantly, we identified a novel lnc-HMOX1-miR-3587-HMOX1 axis, which holds promise as a potential therapeutic target for RIR injury.

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Declaration of competing interest The authors declare that they have no conflict of interest.

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