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
They cannot, however, determine whether systemic sympathetic modulation will produce a clinically meaningful net skeletal benefit in humans, because drug exposure also affects cardiovascular function, perfusion, physical activity, metabolism, stress responses, and fall risk.
方法
We synthesize evidence on skeletal innervation and neurovascular organization, local NE release and clearance, adrenergic receptor signaling, and downstream effects on osteoblast-lineage cells, osteocytes, osteoclast precursors, and marrow niche populations across homeostasis, aging, chronic stress and depression, estrogen deficiency, fracture healing, and cancer-associated bone disease.；Aging is treated as a multilevel modifier involving changes in autonomic rhythmicity, neural integrity, neurovascular coupling, NE handling, receptor responsiveness, marrow adiposity, inflammaging, cellular senescence, and stem-cell competence.；Sympathetic effects are therefore interpreted according to the variable measured, skeletal site, species, disease stage, intervention timing, and systemic context.
核心结论
First, causal effects demonstrated in genetic, pharmacological, or denervation models establish mechanism within the tested species, skeletal site, disease model, dose, and time window, but do not directly predict human therapeutic response.；Third, a clinical recommendation would require prospective human evidence demonstrating skeletal efficacy together with acceptable cardiovascular, respiratory, metabolic, and fall-related safety.；M– indicates that mechanistic grading is not applicable because the claim is explicitly descriptive of human association rather than a mechanistic causal assertion.
局限
However, skeletal outcomes vary with species, skeletal site, disease stage, intervention timing, neural and vascular status, transmitter clearance, physical activity, glucocorticoid exposure, metabolic inflammation, and marrow composition.；Future studies should prioritize age-, sex-, site-, and stage-resolved neural mapping, direct measurement of intraosseous catecholamine dynamics, cell-specific causal interventions, and prospective human skeletal outcomes.；Gut-derived and central serotonergic pathways, together with osteoclast redox–metabolic programming, further broaden the biological context of age-related skeletal decline; however, these mechanisms should not be generalized as direct evidence of altered bone-directed sympathetic signaling in physiological aging [12-14].
对本项目的价值
中等价值：属「免疫衰老与慢性炎症」方向；免疫 / 炎症与衰老栏目可用作本项目文献库与综述素材。 ｜ 价值分 2.7/5（★★★☆☆）
全文来源
出版商/仓储 OA PDF（正文 24,609 字符，题名指纹 1.0，正文内 DOI 命中，已过题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：交感神经对骨代谢的调控：稳态、衰老与疾病中的机制
- 英文标题：Sympathetic Regulation of Bone Metabolism: Mechanisms across Homeostasis, Aging and Disease.
- 期刊与标识：Aging and disease · PMID 42970310 · DOI 10.14336/AD.2026.0886