ReviewBiology2025
Lactate Metabolism: The String-Puller for the Development of Pancreatic Cancer.
Review in Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Lactate-induced epithelial-mesenchymal transition: a metabolic nexus in pancreatic cancer metastasis.Translational cancer research · 2026Review
- Lysine lactylation-mediated post-translational modification: Molecular mechanisms and therapeutic target exploration in tumour drug resistance.Clinical and translational medicine · 2026Review
- Glycolytic lactylation modulates cell death decisions in diabetic kidney disease: Metabolic‑epigenetic interplay between ferroptosis and autophagy in fibrotic remodeling (Review).International journal of molecular medicine · 2026Review
- Lactate-lactylation in tumor angiogenesis and progression: mechanisms, biomarker potential, and therapeutic implications.Biomarker research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Since the discovery of the 'Warburg effect' in cancer, lactate is no longer considered merely a metabolic byproduct. It serves as both a metabolic fuel involved in the energy cycle and a signaling molecule that modulates cellular signal transduction. Recent studies have demonstrated that lactate participates in protein lactylation, regulates energy metabolism, reshapes the tumor microenvironment, and facilitates the metastasis of pancreatic cancer. Therefore, targeting lactate metabolism has emerged as a promising strategy to improve therapeutic efficacy and survival rates in pancreatic cancer. In this review, we outline aberrant lactate metabolism and recent advancements in lactylation, and elucidate the biological functions of lactate metabolism in pancreatic cancer, focusing on metabolic reprogramming, angiogenesis, and immune evasion. Additionally, we discuss diagnostic and therapeutic approaches targeting lactate metabolism in pancreatic cancer. Research in this field is critical for understanding the mechanisms driving pancreatic cancer progression and is anticipated to develop novel therapeutic strategies for clinical practice.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.