Evidence mapPaperPMID 40658167Full record

ArticleClinical and experimental nephrology2025

Mechanism of RBM15 in high glucose-induced pyroptosis of renal tubular epithelial cells.

Jian Lin, Jian-Bo Feng, Jing-Lin Su, Nan Lin, Yin-Sheng Cai, Fei Lv

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Article in Clinical and experimental nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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6 authors.

Jian Lin *Department of Clinical Laboratory, Dongguan Tungwah Hospital, Dongguan, 523129, Guangdong, China.
Jian-Bo Feng *Department of Clinical Laboratory, Dongguan SongShan Lake Tungwah Hospital, No. 1, Kefa Seventh Road, Songshan Lake Science and Technology Park, Dongguan, 523808, Guangdong, China.
Jing-Lin SuDepartment of Clinical Laboratory, Dongguan SongShan Lake Tungwah Hospital, No. 1, Kefa Seventh Road, Songshan Lake Science and Technology Park, Dongguan, 523808, Guangdong, China.
Nan LinDepartment of Clinical Laboratory, Dongguan SongShan Lake Tungwah Hospital, No. 1, Kefa Seventh Road, Songshan Lake Science and Technology Park, Dongguan, 523808, Guangdong, China.
Yin-Sheng CaiDepartment of Clinical Laboratory, Dongguan SongShan Lake Tungwah Hospital, No. 1, Kefa Seventh Road, Songshan Lake Science and Technology Park, Dongguan, 523808, Guangdong, China. xunga35@163.com.
Fei LvDepartment of Clinical Laboratory, Dongguan SongShan Lake Tungwah Hospital, No. 1, Kefa Seventh Road, Songshan Lake Science and Technology Park, Dongguan, 523808, Guangdong, China. lv_fey@163.com.ORCID http://orcid.org/0009-0005-6480-2832

Funding

Dongguan Social Science and Technology Development (General) Project (20231800904962) (20231800939032) (20231800939022) (20231800939232)
6 · The paper itself

Abstract

backgroundDiabetic nephropathy (DN) is the leading cause of end-stage renal disease. We aimed to explore the role of RNA binding motif protein 15 (RBM15) in high glucose (HG)-induced pyroptosis of renal tubular epithelial cell, thus providing theoretical knowledge and new targets for DN treatment.

methodsHG-induced HK-2 cells were used to establish DN cell models. RBM15 expression was inhibited in HK-2 and detected. Cell viability was detected by cell counting kit-8. The levels of NLR family pyrin domain containing 3 (NLRP3), NLR family CARD domain containing 4 (NLRC4), gasdermin D (GSDMD)-N, and cleaved Caspase-1 were detected by Western blot assay. The levels of IL-1β and IL-18 were detected by enzyme linked immunosorbent assay. The enrichment of insulin-like growth factor 2 mRNA binding protein (IGF2BP2) and N6-methyladenosine (m6A) on NLRP3 and NLRC4 were analyzed by methylated RNA immunoprecipitation (MeRIP) and RIP. The stability of NLRP3 and NLRC4 mRNA was analyzed. The mechanism was verified by interfering NLRP3 and NLRC4 expression.

resultsRBM15 was highly expressed in HG-induced HK-2 cells. Inhibition of RBM15 reversed cell viability, inhibited inflammation, and alleviated pyroptosis. RBM15 promoted the expression of inflammasomes NLRP3 and NLRC4 through IGF2BP2-dependent m6A modification.

conclusionRBM15 promoted the expression of inflammasomes NLRP3 and NLRC4 through IGF2BP2-dependent m6A modification, thereby promoting pyroptosis.

Indexed as

Diabetic NephropathiesEpithelial CellsGlucoseKidney TubulesPyroptosisRNA-Binding ProteinsAdenosineCalcium-Binding ProteinsCARD Signaling Adaptor ProteinsCell LineGasderminsHumansInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinPhosphate-Binding ProteinsAdenosineCalcium-Binding ProteinsCARD Signaling Adaptor ProteinsGasderminsGlucoseGSDMD protein, humanInterleukin-18Interleukin-1betaNLRC4 protein, humanNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanN-methyladenosinePhosphate-Binding ProteinsRNA-Binding ProteinsHigh glucoseNLRP3PyroptosisRBM15Renal tubular epithelial cell

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.