ArticleJCI insight2025
Lactate programs PBX1 lactylation and mesangial proliferation in lupus nephritis.
Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Metabolic memory in the kidney: how lactate and lactylation drive the path from acute injury to chronic disease.Renal failure · 2026Review
- Metabolic determinants of autoimmune kidney diseases.Nature reviews. Nephrology · 2026Review
- Article
- Lactate-Mediated Lysine Lactylation in Renal Fibrosis: Current Progress and Challenges.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Crosstalk between lactylation and other post-translational modifications in health and diseases.Molecular biomedicine · 2026Review
- Lactylation in tissue fibrosis: epigenetic mechanisms, metabolic crosstalk, and therapeutic opportunities.Journal of translational medicine · 2026Review
- Dual-mechanistic regulation of podocyte pyroptosis in lupus nephritis by the AP-1 complex: transcriptional activation of NLRP3 and lactate-mediated ubiquitination inhibition.Cell communication and signaling : CCS · 2026Article
- Lactylation as a metabolic-epigenetic switch: Mechanisms and roles in cancer, sepsis, trauma, inflammation, and tissue repair.Biochemistry and biophysics reports · 2026Review
- Role of metabolic reprogramming and lactylation in diabetic nephropathy: molecular mechanisms and therapeutic prospects - a narrative review.Frontiers in endocrinology · 2026Review
- Lactate bridges mesangial cells to the differentiation of follicular helper T cells in lupus nephritis.Nature communications · 2025Article
- Lactylation at the crossroads of immune metabolism and epigenetic regulation: revealing its role in rheumatic immune diseases.Journal of translational medicine · 2025Review
- Enzymatic post-translational modifications of proteins in chronic kidney disease: mechanisms, regulation, and clinical significance.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lupus nephritis (LN) constitutes the most common organ-threatening manifestation of systemic lupus erythematosus (SLE), with the pathological proliferation of mesangial cells (MCs) recognized as a critical factor in its pathogenesis and progression. Self-DNA-containing immune complex (DNA-IC) represents a prime pathogenic factor in SLE, yet its pathological effect on MCs remains unclear. In the present study, we elucidated the mechanism underlying the excessive proliferation of MCs following the recognition of DNA-IC in patients with LN. Here, we pinpointed that the excessive proliferation of MCs was attributed to an anomalous transition from the G1 to the S phase of the cell cycle in patients with LN. Mechanically, the dysfunction of P27 protein resulted in the aberrant G1-S phase transition, and the phenomenon was closely related to the ubiquitin-mediated degradation of its key transcription factor, PBX1. This degradation was regulated by lactylation of PBX1 in the site of Lys40 residue. The elevated lactylation level of PBX1 protein was caused by the upregulation of glycolysis levels induced by DNA-IC. Accordingly, targeting lactate production in MCs from patients with LN effectively alleviated their renal inflammation and fibrosis progression. Elevated lactate resulted in PBX1 lactylation, leading to excessive proliferation of MCs and, thus, serving as a promising therapeutic target for LN.
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Registered trials
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