LncRNA PCED1B-AS1 Inhibits Sepsis-Induced Acute Kidney Injury by Promoting Transformation of Macrophages from M1 to M2 Type via Regulating the miR-361-3p/SOCS1 Axis

Sep 29, 2026

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Sepsis commonly leads to acute kidney injury (AKI) in intensive care patients, characterized by rapid onset, strong inflammation, and poor clinical outcomes. This study measured PCED1B-AS1 in healthy individuals and in sepsis patients with or without AKI, then examined how PCED1B-AS1 influences macrophage polarization. PCED1B-AS1 was downregulated in sepsis without AKI and further reduced in AKI, with low expression linked to worse prognosis. Functional assays showed that PCED1B-AS1 overexpression promoted M1-to-M2 transformation through the miR-361-3p/SOCS1 axis, suppressing apoptosis and inflammatory responses.

LanguageEnglish

CategoryHealthcare

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Pages16

Reading Time40 min

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Patients and Methods

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Journal of Inflammation Research Open Access Full Text Article ORIGINAL RESEARCH LncRNA PCED1B-AS1 Inhibits Sepsis-Induced Acute Kidney Injury by Promoting Transformation of Macrophages from M1 to M2 Type via Regulating the miR-361-3p/SOCS1 Axis Peng Huang 1 , 2 , *, Youfu Li 3 , *, SiDan Wang 1 , YuanYuan Wu 1 , Shengrui Zhang4 1Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise City, Guangxi, People’s Republic of China; 2Key Laboratory of Medical Research Basic Guarantee for Immune-Related Diseases Research of Guangxi, Baise City, Guangxi, People’s Republic of China; 3Department of Critical Care Medicine, Yiyang Central Hospital, Yiyang City, Hubei Province, People’s Republic of China; 4Department of Intensive Care Unit, Ganzhou People’s Hospital, Ganzhou City, Jiangxi Province, People’s Republic of China *These authors contributed equally to this work Correspondence: Shengrui Zhang, Department of Intensive Care Unit, Ganzhou People’s Hospital, No. 16, Meiguan Avenue, Ganzhou City, Jiangxi Province, 341000, People’s Republic of China, [Email Zhangshr_ganzhou@163.com](Email Zhangshr_ganzhou@163.com) | Purpose: A common complication observed in septic patients under intensive care is acute kidney injury (AKI), which is characterized by acute onset and strong inflammation, resulting in poor clinical outcomes for patients. This study aims to explore the expression status of PCED1B-AS1 in sepsis-induced AKI and to preliminarily investigate the molecular mechanism by which PCED1B-AS1 affects AKI. Patients and Methods: This study included 105 healthy individuals and 220 patients with sepsis (110 patients with AKI and 110 non-AKI patients) . The levels of PCED1B-AS1 were examined by RT-qPCR. Macrophage polarization was induced by LPS treatment of RAW264.7 cells, and an in vitro renal injury model was established using HK-2 cells. Cell proliferation ability was evaluated by CCK-8 assay, apoptosis was detected by flow cytometry, and the levels of inflammatory factors were assessed using ELISA kits. The dual-luciferase assay was used to verify the interrelationship among the PCED1B-AS1/miR-361-3p/SOCS1 axis.
Results: PCED1B-AS1 was downregulated in sepsis patients without AKI and further reduced in AKI patients. PCED1B-AS1 could differentiate healthy individuals from non-AKI sepsis patients and identify AKI patients. Additionally, low PCED1B-AS1 expression correlated with poor AKI prognosis. Overexpression of PCED1B-AS1 promoted the polarization of M1 macrophages to M2 by regulating the miR-361-3p/SOCS1 axis, thereby inhibiting apoptosis and inflammatory responses in HK-2 cells.
Conclusion: PCED1B-AS1 may serve as a potential diagnostic and prognostic marker and inhibit sepsis-induced AKI by promoting transformation of macrophages from M1 to M2 type via regulating the miR-361-3p/SOCS1 axis.
Keywords: PCED1B-AS1, miR-361-3p, macrophage polarization, diagnosis, prognosis | | --- | | Introduction
Sepsis is a life-threatening condition characterized by organ dysfunction, stemming from an improperly regulated host reaction to infectious agents, and is associated with an exceptionally high rate of mortality.1 A common complication observed in septic patients under intensive care is acute kidney injury (AKI) .1 The pathophysiological basis underlying sepsis-induced AKI is intricate, encompassing a multitude of factors including modifications in renal hemodynamics, endothelial cell dysfunction, and heightened inflammatory responses.2,3 Regrettably, sepsis-induced AKI carries a very poor prognosis. Additionally, the death rate among sepsis patients with AKI is estimated to be three to five times higher than in non-AKI.4 The prevention of sepsis-induced AKI presents significant challenges, as the majority of patients typically initiate treatment only upon the manifestation of overt clinical signs.5 Consequently, early identification is crucial, enabling the initiation

FAQs

What is the main purpose of the study on PCED1B-AS1 in sepsis-induced AKI?

The study evaluates PCED1B-AS1 expression in sepsis-induced AKI and investigates the molecular mechanism by which PCED1B-AS1 affects AKI.

How were PCED1B-AS1 levels and macrophage polarization assessed?

PCED1B-AS1 levels were measured using RT-qPCR, while macrophage polarization was induced in RAW264.7 cells with LPS. In vitro renal injury used HK-2 cells.

What mechanism links PCED1B-AS1 to AKI outcomes?

PCED1B-AS1 regulates the miR-361-3p/SOCS1 axis to promote transformation of macrophages from M1 to M2 type, inhibiting apoptosis and inflammatory responses.

Sep 29, 2026

Uploaded by Ezra