---
title: "SIRT2 inhibition reduces sepsis-associated AKI by NEU1 acetylation and CD44/PI3K/AKT pathway activ"
id: "pubmed-42361896"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42361896"
content_type: "clinical_feed_article"
specialty: "Critical Care"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42361896/"
doi: "10.1016/j.lfs.2026.124554"
published_at: "2026-09-15T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# SIRT2 inhibition reduces sepsis-associated AKI by NEU1 acetylation and CD44/PI3K/AKT pathway activ
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42361896
- **Specialty:** [Critical Care](https://medichelpline.com/clinical-feed/critical-care.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42361896/)
- **DOI:** [10.1016/j.lfs.2026.124554](https://doi.org/10.1016%2Fj.lfs.2026.124554)
- **Published At:** 2026-09-15T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Aim: to evaluate the role of **SIRT2** in renal injury and inflammation in sepsis-associated acute kidney injury (**S-AKI**) and to test whether pharmacological inhibition confers protection. - Models: lipopolysaccharide (LPS)-induced S-AKI in wild-type and SIRT2 whole-body knockout mice; HK-2 human renal tubular epithelial cells with SIRT2 knockdown or overexpression. - Outcomes assessed: renal histology, biochemical indices, pro-inflammatory cytokines, macrophage infiltration, cell death, NEU1 acetylation and sialidase activity, CD44 sialylation and binding to hyaluronic acid (HA), and downstream **PI3K/AKT** signaling. - Key mechanistic finding: **SIRT2** deacetylates NEU1 at lysine 395; SIRT2 inhibition leads to NEU1 hyperacetylation, reduced NEU1 sialidase activity, increased CD44 sialylation and CD44/HA binding, and activation of the **CD44/PI3K/AKT** pathway associated with renal protection. - Genetic evidence: SIRT2 whole-body knockout mice showed markedly less renal damage and lower levels of pro-inflammatory cytokines in the LPS S-AKI model. - Cellular evidence: SIRT2 knockdown in HK-2 cells attenuated LPS-induced inflammation and cell death; SIRT2 overexpression exacerbated inflammatory responses and cell death. - Pharmacology: the selective SIRT2 inhibitor **AGK2** mitigated LPS-induced renal injury and inflammation in mice; a **Nano-AGK2** formulation showed improved renal accumulation and greater therapeutic efficacy versus free AGK2. - Implication: SIRT2 acts as a post-translational regulator in S-AKI, and inhibiting SIRT2 is proposed as a potential therapeutic strategy that warrants further preclinical study. - Limitations: the abstract reports methods and outcomes but does not provide detailed numeric results, dosing regimens, safety data, or long-term outcomes; those details were not reported in the source abstract.
## Clinical Analysis & Structured Key Points
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Epub 2026 Jun 26. # Inhibiting SIRT2 attenuates sepsis-associated acute kidney injury via NEU1 acetylation-mediated CD44/PI3K/AKT pathway activation [Yaqiong Jiang](https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+Y&cauthor_id=42361896)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#full-view-affiliation-1 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China."), [Dan Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+D&cauthor_id=42361896)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#full-view-affiliation-1 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China."), [Li Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+L&cauthor_id=42361896)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#full-view-affiliation-1 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China."), [Zishun Zhan](https://pubmed.ncbi.nlm.nih.gov/?term=Zhan+Z&cauthor_id=42361896)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#full-view-affiliation-1 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China."), [Zhijun Huang](https://pubmed.ncbi.nlm.nih.gov/?term=Huang+Z&cauthor_id=42361896)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#full-view-affiliation-2 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China; Furong Laboratory, Changsha, Hunan, China."), [Bin Yi](https://pubmed.ncbi.nlm.nih.gov/?term=Yi+B&cauthor_id=42361896)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#full-view-affiliation-3 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China. Electronic address: yibin2008@csu.edu.cn.") Affiliations Expand ### Affiliations * 1 Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China. * 2 Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China; Furong Laboratory, Changsha, Hunan, China. * 3 Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China. Electronic address: yibin2008@csu.edu.cn. * PMID: **42361896** * DOI: [ 10.1016/j.lfs.2026.124554 ](https://doi.org/10.1016/j.lfs.2026.124554) Item in Clipboard # Inhibiting SIRT2 attenuates sepsis-associated acute kidney injury via NEU1 acetylation-mediated CD44/PI3K/AKT pathway activation Yaqiong Jiang et al. Life Sci. 2026. Show details Display options Display options Format Abstract PubMed PMID Life Sci Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Life+Sci%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Life+Sci%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42361896/) . 2026 Sep 15:401:124554. doi: 10.1016/j.lfs.2026.124554. Epub 2026 Jun 26. ### Authors [Yaqiong Jiang](https://pubmed.ncbi.nlm.nih.gov/?term=Jiang+Y&cauthor_id=42361896)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#short-view-affiliation-1 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China."), [Dan Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+D&cauthor_id=42361896)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#short-view-affiliation-1 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China."), [Li Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+L&cauthor_id=42361896)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#short-view-affiliation-1 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China."), [Zishun Zhan](https://pubmed.ncbi.nlm.nih.gov/?term=Zhan+Z&cauthor_id=42361896)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#short-view-affiliation-1 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China."), [Zhijun Huang](https://pubmed.ncbi.nlm.nih.gov/?term=Huang+Z&cauthor_id=42361896)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#short-view-affiliation-2 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China; Furong Laboratory, Changsha, Hunan, China."), [Bin Yi](https://pubmed.ncbi.nlm.nih.gov/?term=Yi+B&cauthor_id=42361896)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42361896/#short-view-affiliation-3 "Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China. Electronic address: yibin2008@csu.edu.cn.") ### Affiliations * 1 Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China. * 2 Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China; Furong Laboratory, Changsha, Hunan, China. * 3 Department of Nephrology, The Third Xiangya Hospital, Central South University, 138 Tongzipo Rd, Changsha, Hunan, 410013, China; Clinical Research Center for Critical Kidney Disease in Hunan Province, Changsha, China. Electronic address: yibin2008@csu.edu.cn. * PMID: **42361896** * DOI: [ 10.1016/j.lfs.2026.124554 ](https://doi.org/10.1016/j.lfs.2026.124554) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract **Aims:** Sepsis-associated acute kidney injury (S-AKI) is a severe complication of sepsis, characterized by high morbidity and mortality, yet lacks effective treatment options in clinical practice. This study aims to investigate the role of SIRT2 in mediating renal injury and inflammation in S-AKI. **Materials and methods:** LPS-induced S-AKI models were established in wild-type and SIRT2 whole-body knockout mice, as well as in HK-2 cells with SIRT2 knockdown or overexpression. Renal injury, inflammatory cytokines, macrophage infiltration, and cell death were evaluated by histological, biochemical, and molecular analyses. NEU1 acetylation, sialidase activity, CD44 sialylation, and downstream PI3K/AKT signaling were further examined. Pharmacological inhibition studies in mice were performed using SIRT2 selective inhibitor AGK2 and a nano-formulation of AGK2 (Nano-AGK2). **Key findings:** We found that SIRT2 whole-body knockout significantly alleviated renal damage and reduced pro-inflammatory cytokines in S-AKI. Knockdown of SIRT2 attenuated LPS-induced inflammation and cell death in HK-2 cells, whereas its overexpression exacerbated the inflammatory response and cell death. Mechanistically, SIRT2 was shown to deacetylate NEU1 at lysine 395. Inhibiting SIRT2 caused hyperacetylated NEU1, which reduced NEU1 sialidase activity and enhanced CD44 sialylation and CD44/HA binding, promoting PI3K/AKT signaling and renal protection. Furthermore, pharmacological inhibition using AGK2 mitigated LPS-induced renal injury and inflammation, while Nano-AGK2 exhibited enhanced renal accumulation and therapeutic efficacy compared to free AGK2. **Significance:** These findings identify SIRT2 as a novel post-translational regulator in S-AKI, suggesting that SIRT2 inhibition may serve as a potential therapeutic target for S-AKI, which deserves further preclinical investigation. **Keywords:** Acute kidney injury; Inflammation; NEU1; SIRT2. Copyright © 2026 Elsevier Inc. All rights reserved. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declaration of competing interest The authors declare that they have no competing interests. ## Similar articles * [ INHIBITING SIRT2 ATTENUATES SEPSIS-INDUCED ACUTE KIDNEY INJURY VIA FOXO1 ACETYLATION-MEDIATED AUTOPHAGY ACTIVATION. ](https://pubmed.ncbi.nlm.nih.gov/39527461/) Yu B, Weng L, Li J, Wang T, Qiu W, Li Y, Shi M, Lin B, Lin X, Chen Z, Zeng Z, Gao Y.Yu B, et al.Shock. 2025 Feb 1;63(2):255-266. doi: 10.1097/SHK.0000000000002505. Epub 2024 Nov 8.Shock. 2025.PMID: 39527461Free PMC article. * [ HBP21 Alleviates Sepsis-Induced Acute Kidney Injury by Targeting PI3K/AKT-Mediated M1 Macrophage Polarization. ](https://pubmed.ncbi.nlm.nih.gov/40757051/) An N, Xu M, Chen R, Wang C, Bai Y.An N, et al.Mediators Inflamm. 2025 Jul 27;2025:9021628. doi: 10.1155/mi/9021628. eCollection 2025.Mediators Inflamm. 2025.PMID: 40757051Free PMC article. * [ PGAM5 modulates PI3K/AKT/mTOR-dependent mitochondrial homeostasis in sepsis-induced acute kidney injury. ](https://pubmed.ncbi.nlm.nih.gov/41985761/) Jin X, Sheng L, Jiang D, Tian D, Jia H, Wu X.Jin X, et al.Toxicol Appl Pharmacol. 2026 Jun;511:117812. doi: 10.1016/j.taap.2026.117812. Epub 2026 Apr 13.Toxicol Appl Pharmacol. 2026.PMID: 41985761 * [ RPS3 Aggravates Sepsis-Induced Acute Kidney Injury Through Activating NF-kappaB Mediated Renal Inflammatory Responses. ](https://pubmed.ncbi.nlm.nih.gov/41811702/) Zhang X, Ma Q, Wang J, Zhang Z, Zhang J.Zhang X, et al.Physiol Res. 2026 Mar 11;75(1):63-77. doi: 10.33549/physiolres.935642.Physiol Res. 2026.PMID: 41811702Free PMC article. * [ Allicin Attenuates Sepsis-Induced Acute Kidney Injury by Inhibiting Pyroptosis Through Negative Regulation of the PI3K/AKT Pathway. ](https://pubmed.ncbi.nlm.nih.gov/41953959/) Zheng Y, Li S, Zhu L, Zhang L.Zheng Y, et al.Mediators Inflamm. 2026;2026(1):e5454020. doi: 10.1155/mi/5454020.Mediators Inflamm. 2026.PMID: 41953959Free PMC article. [ See all similar articles ](https://pubmed.ncbi.nlm.nih.gov/?linkname=pubmed_pubmed&from_uid=42361896) ## MeSH terms * Acetylation / drug effects Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Acetylation%2Fdrug+effects%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Acetylation) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42361896/) * Acute Kidney Injury* / etiology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Acute+Kidney+Injury%2Fetiology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Acute+Kidney+Injury) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42361896/) * Acute Kidney Injury* / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Acute+Kidney+Injury%2Fmetabolism%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Acute+Kidney+Injury) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42361896/) * Acute Kidney Injury* / pathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Acute+Kidney+Injury%2Fpathology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Acute+Kidney+Injury) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42361896/) * Acute Kidney Injury* / prevention & control Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Acute+Kidney+Injury%2Fprevention+and+control%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Acute+Kidney+Injury) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42361896/) * Animals Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Animals%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Animals) * [ Add to Search ](https://
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