时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
Based on these alterations, we further explored whether the metabolic changes in NAD+ during age-related AF were regulated by NAMPT and investigated the underlying mechanisms.；Various animal AF models have been developed, each with its own limitations and advantages depending on specific research objectives and conditions.Four types of remodeling-electrical, structural, autonomic nervous system, and energy metabolism-are crucial in AF onset and progression.；Future studies using atrial-specific genetic interventions or inducible conditional knockout models will be necessary to more definitively determine whether atrial metabolic dysregulation is a causal driver of AF development, while minimizing the potential confounding effects of systemic physiological disturbances.Thirdly, NAD+ metabolism and CLOCK influence each other, with SIRT1 as the link, forming the ‘NAD+-SIRT1-CLOCK/BMAL1-NAMPT-NAD+’ loop.
方法
Due to increased human longevity and enhanced screening, the incidence of AF is expected to rise by 2.3 times, placing a heavy burden on patients, doctors, and medical systems [3, 4].；However, the effects and mechanisms of CARM1 on CLOCK and NAMPT in regulating NAD+ in age-related AF are still unclear.This study first observed a downregulation of NAD+ and NAMPT levels in the left atrial appendage of patients with AF, accompanied by a decrease in ATP content.；Based on these alterations, we further explored whether the metabolic changes in NAD+ during age-related AF were regulated by NAMPT and investigated the underlying mechanisms.
核心结论
Research indicates that under steroid hormone stimulation, CARM1 can be recruited by steroid receptor coactivator-3 (SRC-3) to regulate target gene transcription by methylating arginine residues on chromatin histones.；Masson’s staining demonstrated the presence of collagen deposition and fibrosis in the Adult AF group, whereas the Aging AF group showed extensive collagen accumulation accompanied by severe fibrosis (Fig. 2E-H).；These findings indicated that atrial enlargement and decreased LVEF were most pronounced in the Aging AF group.
局限
However, studies about energy metabolic remodeling in age-related AF is still expected.Currently, studies indicate that abnormal myocardial energy metabolism is a key factor in AF onset and maintenance [7].；However, the regulatory mechanism by which NAD+ deficiency contributes to atrial metabolic remodeling and promotes age-related AF remains incompletely understood.Nicotinamide phosphoribosyl transferase (NAMPT) is a rate-limiting enzyme in the NAD+ salvage biosynthetic pathway.；However, the effects and mechanisms of CARM1 on CLOCK and NAMPT in regulating NAD+ in age-related AF are still unclear.This study first observed a downregulation of NAD+ and NAMPT levels in the left atrial appendage of patients with AF, accompanied by a decrease in ATP content.
对本项目的价值
中等价值：属「代谢 / 内分泌 / 肝肾老化」方向；代谢 / 内分泌 / 肝肾老化的界面栏目可用作本项目文献库与综述素材。 ｜ 价值分 2.6/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 55,178 字符，题名指纹 0.83，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：NAMPT 依赖的 NAD+ 下降驱动年龄相关房颤的能量代谢改变
- 英文标题：NAMPT-dependent NAD(+) decline drives energy metabolism changes in aging-related atrial fibrillation.
- 期刊与标识：BMC medicine · PMID 42972381 · DOI 10.1186/s12916-026-05108-z · PMC PMC13726150