| 引用本文: |
吴源陶, 傅馨莹, 王智槟, 邹晓玲, 邹译娴.从“虚损痨瘵，燮理气阴”探讨糖尿病肾病铁死亡病机及防治思路[J].湖南中医药大学学报,2026,46(1):126-133[点击复制] |
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| 从“虚损痨瘵，燮理气阴”探讨糖尿病肾病铁死亡病机及防治思路 |
| 吴源陶,傅馨莹,王智槟,邹晓玲,邹译娴 |
| (湖南中医药大学第一附属医院, 湖南 长沙 410007;湖南中医药大学, 湖南 长沙 410208) |
| 摘要: |
| 本文基于“虚损痨瘵，燮理气阴”理论，探讨糖尿病肾病以铁死亡为核心的病理机制与防治策略。脾肾两虚为本，湿热、痰瘀、浊毒为标，共同导致铁稳态失衡，表现为溶质载体家族7成员11（SLC7A11，又名xCT）、长链酰基辅酶A合成酶家族成员4（GPX4）下调与长链酰基辅酶A合成酶家族成员4（ACSL4）上调，诱发脂质过氧化与铁死亡，损伤肾小管上皮及足细胞；进而通过损伤相关分子模式（DAMPs）、转化生长因子-β（TGF-β）/Smad及Nod样受体蛋白3（NLRP3）信号促进成纤维细胞活化与胶原沉积，导致肾纤维化。遵循“治未病”理念，提出三级防治策略：早期健脾益气养阴并化湿，联合抗氧化与抗铁死亡，延缓微量白蛋白尿出现；中期清热解毒、活血通络，协同调控核因子E2相关因子2（Nrf2）/GPX4与ACSL4及TGF-β/Smad轴，抑制炎症与纤维化放大；后期扶正培本、温阳利水，兼顾解毒通络与肾脏保护，改善症状与预后。 |
| 关键词: 糖尿病肾病 铁死亡 虚损痨瘵 燮理气阴 脾肾两虚 溶质载体家族7成员11 长链酰基辅酶A合成酶家族成员4 |
| DOI：10.3969/j.issn.1674-070X.2026.01.017 |
| 投稿时间：2025-09-27 |
| 基金项目:湖南省自然科学基金面上项目（2024JJ5317）；湖南省教育厅资助科研项目（25A0293）。 |
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| Pathogenesis and prevention-treatment strategies of ferroptosis in diabetic kidney disease from the perspective of "treating consumptive deficiency by harmonizing qi and yin" |
| WU Yuantao, FU Xinying, WANG Zhibin, ZOU Xiaoling, ZOU Yixian |
| (The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, China;Hunan University of Chinese Medicine, Changsha, Hunan 410208, China) |
| Abstract: |
| Based on the theory of "treating consumptive deficiency by harmonizing qi and yin", this paper explores ferroptosis-centered pathological mechanisms and corresponding prevention and treatment strategies for diabetic kidney disease (DKD). Deficiency of the spleen and kidney serves as the root cause, while damp-heat, phlegm-stasis, and turbidity-toxin represent the manifestations. Together, these factors disrupt iron homeostasis, characterized by downregulation of solute carrier family 7 member 11 (SLC7A11, xCT) and glutathione peroxidase 4 (GPX4) and upregulation of long-chain acyl-CoA synthetase family member 4 (ACSL4). These imbalance triggers lipid peroxidation and ferroptosis, damaging renal tubular epithelial cells and podocytes. Subsequently, through damage-associated molecular patterns (DAMPs), transforming growth factor-β (TGF-β)/Smad, and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) signaling pathways, it promotes fibroblast activation and collagen deposition, ultimately leading to renal fibrosis. Guided by the concept of "preventing a disease before it arises", a three-tier prevention and treatment strategy is proposed: in the early stage, strengthening the spleen, replenishing qi, nourishing yin, and transforming dampness, combined with antioxidant and anti-ferroptotic interventions, to delay the onset of microalbuminuria; during the moderate stage, clearing heat and removing toxins, circulating blood and unblocking collaterals, while synergistically modulating the nuclear factor E2-related factor 2 (Nrf2)/GPX4, ACSL4, as well as the TGF-β/Smad axis, to suppress inflammation and fibrosis amplification; in the late stage, reinforcing healthy qi, consolidating the root, warming yang and disinhibiting water, while integrating toxin removing, collateral unblocking, and renal protection, to alleviate symptoms and improve prognosis. |
| Key words: diabetic kidney disease ferroptosis consumptive deficiency harmonizing qi and yin deficiency of the spleen and kidney solute carrier family 7 member 11 long-chain acyl-CoA synthetase family member 4 |
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