时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
By consolidating current knowledge on glycolysis‑centric meta‑ bolic underpinnings of PF, this review underscores the promise of metabolism‑based interventions and discusses challenges for translating these findings into effective therapies.；Glycolysis‑related signaling pathways and PF 6. Interaction between glycolysis and other metabolic pathways 7. Therapeutic strategies and challenges of targeting glycolysis in PF 8.；As a basket term encompassing a spectrum of fibrotic lung diseases, PF includes idiopathic PF (IPF), of unknown etiology with a usual interstitial pneumonia pattern, as well as secondary forms attributable to known causes, including occupational and environmental exposures, drug toxicities, connective tissue diseases and infections (2).
方法
Concurrently, the accu‑ mulation of senescent epithelial cells and fibroblasts amplifies pro‑fibrotic signaling via the senescence‑associated secretory phenotype, thereby further reinforcing the pro‑fibrotic milieu and sustaining aberrant repair pathways (11,12).；At the molecular and cellular levels, senescent epithelial cells and fibroblasts acquire a senescence‑associated secretory phenotype, sustaining profibrotic signaling, activating fibroblasts and promoting ECM deposition (11,33).；One such disorder, gastro‑esophageal reflux disease (GERD), is commonly observed in IPF and is hypothesized to exac‑ erbate disease progression through chronic microaspiration of gastric contents, thereby sustaining alveolar epithelial injury and promoting profibrotic repair mechanisms (59).
核心结论
By consolidating current knowledge on glycolysis‑centric meta‑ bolic underpinnings of PF, this review underscores the promise of metabolism‑based interventions and discusses challenges for translating these findings into effective therapies.；Introduction Pulmonary fibrosis (PF) is a chronic, progressive interstitial lung disease characterized primarily by pathologically defined aberrant tissue repair, accumulation of activated fibroblasts and excessive deposition of extracellular matrix (ECM), which collectively lead to irreversible architectural distortion and loss of lung function (1).；PF represents the final common pathway of multiple interstitial lung diseases (ILDs) and is associated with substantial morbidity and mortality world‑ wide. ‖ 结论：Collectively, these metabolic shifts facilitate fibroblast‑to‑myofibroblast differentiation, promote ECM deposition and disrupt immune cell functions and energy homeostasis, thereby driving the fibrotic process.
局限
Despite these advancements, the side effects and restricted efficacy of current antifibrotic agents, coupled with the lack of therapies that can halt or reverse fibrotic lung damage, highlight the pressing need for innovative therapeutic strategies.；Building on this mechanistic understanding, the current study highlights metabolic targets with drug devel‑ opment potential, including glucose transporters (GLUTs), glycolytic rate‑limiting enzymes and critical metabolic intermediates.；Another well‑established fibro‑ genic agent is asbestos, whose role warrants further scrutiny; chronic inhalation of its fibers, such as chrysotile and crocido‑ lite, can cause asbestosis, a fibrotic lung disease
对本项目的价值
★☆☆☆☆ 代谢轴既干预敏感性最高，也是老药新用供给最充足的来源。
全文来源
出版商 OA PDF（正文 148,741 字符，已过 DOI 逐字 / 标题指纹归属校验）
原文题录
- 英文标题：Glycolysis in pulmonary fibrosis: From drivers to therapeutic opportunities (Review).
- 期刊与标识：Int J Mol Med · PMID 42960450 · DOI 10.3892/ijmm.2026.6031
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