ArticleFrontiers in pharmacology2026
Integrated transcriptomics identifies ER stress-associated apoptosis in post-resuscitation AKI and supports early Dl-3-n-butylphthalide-associated renoprotection in a porcine TCA model.
Article in Frontiers in pharmacology, 2026. 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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Abstract
Background: Dl-3-n-butylphthalide (NBP) is a small-molecule compound derived from celery seeds with anti-inflammatory, antioxidant, and anti-apoptotic properties. Although NBP has shown protective effects in various kidney diseases, its role in traumatic cardiac arrest (TCA)-induced acute kidney injury (AKI) remains unclear. This study aimed to investigate the effects of NBP on AKI following TCA in pigs and to determine whether these effects were associated with modulation of ERS/UPR-associated apoptotic readouts. Methods: We integrated ischemia-reperfusion injury (IRI)-related bulk transcriptomic/microarray datasets with single-cell RNA sequencing (scRNA-seq) data. Differential expression analysis, Hallmark GSEA, and GSVA/ssGSEA were performed to quantify unfolded protein response (UPR) and apoptosis, focusing on proximal tubule (PT) cells via PT-state stratification, pseudo-bulk differential analysis, and pseudotime inference. For Results: Integrated bulk, single-cell, PT-state, pseudotime, and PT pseudo-bulk analyses prioritized a PT-enriched PERK-ATF4-CHOP-associated stress-apoptosis module, predominantly within injury-associated PT states. Along PT injury-state progression, HSPA5/GRP78, PERK/EIF2AK3, ATF4, CHOP/DDIT3, and apoptosis-related effectors showed coordinated transcript-level remodeling, suggesting engagement of an ERS/UPR-associated stress-apoptosis program rather than establishing pathway causality. Compared with TCA, NBP significantly reduced Cr and BUN, alleviated histopathologic injury, decreased KIM-1/NGAL expression, reduced TUNEL-positive cells and caspase-3 abundance, and was associated with lower PERK, CHOP, and caspase-12 protein expression. Conclusion: A PT-enriched PERK-ATF4-CHOP-associated ERS/UPR stress-apoptosis module was prioritized in injury-associated proximal tubule states during IRI-related AKI. In a porcine TCA model, NBP was associated with reduced early AKI severity within a 24 h observation window, accompanied by lower PERK/CHOP/caspase-related ERS/UPR-associated and apoptosis-related readouts.
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