Article(id=1276203042185810903, tenantId=1146029695717560320, journalId=1146031591421210625, issueId=1276202956391313894, articleNumber=null, orderNo=null, doi=10.3981/j.issn.1000-7857.2025.05.00019, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1746547200000, receivedDateStr=2025-05-07, revisedDate=1762963200000, revisedDateStr=2025-11-13, acceptedDate=null, acceptedDateStr=null, onlineDate=1782200115962, onlineDateStr=2026-06-23, pubDate=1781280000000, pubDateStr=2026-06-13, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782200115962, onlineIssueDateStr=2026-06-23, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782200115962, creator=13701087609, updateTime=1782200115962, updator=13701087609, issue=Issue{id=1276202956391313894, tenantId=1146029695717560320, journalId=1146031591421210625, year='2026', volume='44', issue='11', pageStart='1', pageEnd='136', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1782200095507, creator=13701087609, updateTime=1782200147766, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1276203176344810276, tenantId=1146029695717560320, journalId=1146031591421210625, issueId=1276202956391313894, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276203176344810277, tenantId=1146029695717560320, journalId=1146031591421210625, issueId=1276202956391313894, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=69, endPage=76, ext={EN=ArticleExt(id=1276203042605241305, articleId=1276203042185810903, tenantId=1146029695717560320, journalId=1146031591421210625, language=EN, title=Molecular mechanism of AMPK mediates the mitochondrial autophagy pathway to regulate the physiological health in animals, columnId=1150494642224591153, journalTitle=Science & Technology Review, columnName=Exclusive, runingTitle=null, highlight=null, articleAbstract=

With the transition of China's animal husbandry towards intensification, investigating physiological regulatory mechanisms at the cellular level is of great significance for ensuring animal health and improving production efficiency. As a key intracellular energy sensor, AMP−activated protein kinase (AMPK) plays a multidimensional regulatory role in the process of mitophagy to maintain cellular homeostasis. AMPK can not only directly regulate mitophagy but also influence it through downstream signaling pathways such as ULK1, PGC−1α, and mTOR. This review systematically summarizes the molecular mechanisms by which AMPK mediates mitophagy and its role in animal physiological health. It elaborates on the structure, function, and activation mechanisms of AMPK, as well as its regulation of mitophagy through both direct (e.g., phosphorylating MFF, activating TBK1) and indirect pathways (modulating ULK1, PGC−1α, and mTOR signaling). The synergistic protective effects of AMPK and mitophagy under conditions such as nutrient deficiency, oxidative stress, and disease infection are analyzed. Furthermore, the positive impacts of this regulatory axis on animal muscle development, meat quality, antioxidant capacity, and immune function are discussed. The aim is to provide a scientific theoretical basis for promoting healthy animal growth through the exploration of physiological regulatory mechanisms..

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随着中国畜牧养殖转型,从细胞层面探究生理调控机制对保障动物健康、提升生产效益具有重要意义。综述了AMP激活的蛋白激酶(AMP−activated protein kinase,AMPK)介导线粒体自噬的分子机制及其在动物生理健康中的作用,详细阐述了AMPK的结构功能、激活机制及其通过直接(如磷酸化MFF、激活TBK1)和间接(调控ULK1、PGC−1α和mTOR通路)途径调控线粒体自噬的过程;分析了在营养缺乏、氧化应激及疾病感染等条件下,AMPK与线粒体自噬的协同保护作用:AMPK作为细胞内关键的能量感受器,在线粒体自噬维持细胞稳态过程中发挥多维度的重要调控作用。AMPK不仅可直接调控线粒体自噬,还能通过调节ULK1、PGC−1α和mTOR等下游信号通路影响线粒体自噬。探讨了该调控轴对动物肌肉发育、肉品质、抗氧化应激能力及免疫功能的积极影响,以期为通过探究生理调控机制,促进动物健康生长提供科学理论依据。

, correspAuthors=null, authorNote=null, correspAuthorsNote=null, copyrightStatement=版权所有,未经授权,不得转载。, copyrightOwner=《科技导报》编辑部, extLink=null, articleAbsUrl=null, sourceXml=s+1hgKgOPqUDrVMtokxHqg==, magXml=mHf9JPqZT6wMd3pi6UX47Q==, pdfUrl=null, pdf=EIlLWKAIdnVZxGdnp/i/yw==, pdfFileSize=974828, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=rtQ4c4fD3aG3FgBz8ZnkEg==, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=73iNx1Pi8Zx16LVuxduCxg==, mapNumber=null, authorCompany=null, fund=null, authors=

刘明,教授,研究方向为动物营养与天然功能成分,电子信箱:

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刘明,教授,研究方向为动物营养与天然功能成分,电子信箱:

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刘明,教授,研究方向为动物营养与天然功能成分,电子信箱:

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AMPK介导线粒体自噬的分子机制及其调控动物生理健康的作用
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刘明 1 , 郑茗卉 1 , 张董燕 2
科技导报 | 特色专题 2026,44(11): 69-76
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科技导报 | 特色专题 2026, 44(11): 69-76
AMPK介导线粒体自噬的分子机制及其调控动物生理健康的作用
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刘明1 , 郑茗卉1, 张董燕2
作者信息
  • 1北京农学院动物科学技术学院,北京 102206
  • 2北京市农林科学院畜牧兽医研究所,北京 100097
  • 刘明,教授,研究方向为动物营养与天然功能成分,电子信箱:

Molecular mechanism of AMPK mediates the mitochondrial autophagy pathway to regulate the physiological health in animals
Ming LIU1 , Minghui ZHENG1, Dongyan ZHANG2
Affiliations
  • 1Academy of Animal Science and Technology, Beijing University of Agriculture, Beijing 102206, China
  • 2Institute of Animal Husbandry and Veterinary Medicine, Beijing Academy of Agriculture and Forestry Sciences, Beijing 100097, China
出版时间: 2026-06-13 doi: 10.3981/j.issn.1000-7857.2025.05.00019
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随着中国畜牧养殖转型,从细胞层面探究生理调控机制对保障动物健康、提升生产效益具有重要意义。综述了AMP激活的蛋白激酶(AMP−activated protein kinase,AMPK)介导线粒体自噬的分子机制及其在动物生理健康中的作用,详细阐述了AMPK的结构功能、激活机制及其通过直接(如磷酸化MFF、激活TBK1)和间接(调控ULK1、PGC−1α和mTOR通路)途径调控线粒体自噬的过程;分析了在营养缺乏、氧化应激及疾病感染等条件下,AMPK与线粒体自噬的协同保护作用:AMPK作为细胞内关键的能量感受器,在线粒体自噬维持细胞稳态过程中发挥多维度的重要调控作用。AMPK不仅可直接调控线粒体自噬,还能通过调节ULK1、PGC−1α和mTOR等下游信号通路影响线粒体自噬。探讨了该调控轴对动物肌肉发育、肉品质、抗氧化应激能力及免疫功能的积极影响,以期为通过探究生理调控机制,促进动物健康生长提供科学理论依据。

AMPK  /  线粒体自噬  /  能量代谢  /  细胞稳态  /  动物健康

With the transition of China's animal husbandry towards intensification, investigating physiological regulatory mechanisms at the cellular level is of great significance for ensuring animal health and improving production efficiency. As a key intracellular energy sensor, AMP−activated protein kinase (AMPK) plays a multidimensional regulatory role in the process of mitophagy to maintain cellular homeostasis. AMPK can not only directly regulate mitophagy but also influence it through downstream signaling pathways such as ULK1, PGC−1α, and mTOR. This review systematically summarizes the molecular mechanisms by which AMPK mediates mitophagy and its role in animal physiological health. It elaborates on the structure, function, and activation mechanisms of AMPK, as well as its regulation of mitophagy through both direct (e.g., phosphorylating MFF, activating TBK1) and indirect pathways (modulating ULK1, PGC−1α, and mTOR signaling). The synergistic protective effects of AMPK and mitophagy under conditions such as nutrient deficiency, oxidative stress, and disease infection are analyzed. Furthermore, the positive impacts of this regulatory axis on animal muscle development, meat quality, antioxidant capacity, and immune function are discussed. The aim is to provide a scientific theoretical basis for promoting healthy animal growth through the exploration of physiological regulatory mechanisms..

AMPK  /  mitophagy  /  energy metabolism  /  cellular homeostasis  /  animal health
刘明, 郑茗卉, 张董燕. AMPK介导线粒体自噬的分子机制及其调控动物生理健康的作用. 科技导报, 2026 , 44 (11) : 69 -76 . DOI: 10.3981/j.issn.1000-7857.2025.05.00019
Ming LIU, Minghui ZHENG, Dongyan ZHANG. Molecular mechanism of AMPK mediates the mitochondrial autophagy pathway to regulate the physiological health in animals[J]. Science & Technology Review, 2026 , 44 (11) : 69 -76 . DOI: 10.3981/j.issn.1000-7857.2025.05.00019
中国畜牧产业正逐步向规模化、集约化发展,深入探究动物体内细胞层面的生理调控机制对于提升养殖效益、保障动物健康以及优化繁殖性能等有着至关重要的意义。细胞内能量代谢是维持动物生命活动的核心环节,线粒体作为细胞的能量工厂,其功能状态直接决定了机体能量产生的效率和质量。线粒体自噬(mitophagy)作为细胞选择性清除受损或多余线粒体的关键质量监控机制,在维持细胞稳态中扮演着至关重要的角色。AMP激活的蛋白激酶(AMP−activated protein kinase,AMPK)作为细胞内敏锐的能量状态感受器,不仅能够感知能量变化并启动调控机制,更被发现是线粒体自噬的核心调控者[1]。Egan等[2]发现AMPK可直接磷酸化自噬启动激酶ULK1,将AMPK活性与自噬启动直接联系起来。2016年,Toyama等[3]对AMPK在线粒体分裂中的新功能做了评述,介绍了AMPK通过磷酸化线粒体分裂因子(mitochondrial fission factor,MFF)促进线粒体分裂的机制,为AMPK介导的质量控制提供了新视角。2018年,Herzig等[4]系统阐述了AMPK作为“代谢和线粒体稳态守护者”的多重功能,标志着AMPK与线粒体关系的研究进入系统化阶段。尽管AMPK在能量应激诱导的线粒体自噬中作用已被初步阐明,但其在程序性线粒体自噬(如发育和组织分化中清除功能性线粒体)中的作用却知之甚少。研究发现,AMPK对线粒体自噬的调控存在双重作用:一方面促进损伤诱导的线粒体自噬,另一方面抑制NIX介导的程序性线粒体自噬[5]。这种看似矛盾的功能提示AMPK对线粒体自噬的调控具有更高层次的复杂性和依赖性。本文概述了AMPK与线粒体自噬之间的相互关系及复杂的作用方式,有助于从分子层面揭示动物生理调控机制,进而为畜牧生产实践提供科学依据。
AMPK是一种高度保守的异源三聚体蛋白激酶,主要由催化亚基α、调节亚基β和γ组成[6]。其中,催化亚基α含有激酶活性结构域,是发挥磷酸化作用的关键部位;调节亚基β起到桥梁连接的作用,协助α亚基与γ亚基之间的相互作用以及整个复合物的稳定;γ亚基则是负责感知细胞内单磷酸腺苷(adenosine monophosphate,AMP)、腺嘌呤核苷三磷酸(adenosine triphosphate,ATP)和腺苷二磷酸(adenosine diphosphate,ADP)等腺苷酸变化的重要结构域,它能够通过结合不同的核苷酸来调节AMPK全酶的活性状态[4]。AMPK在细胞代谢和应激中能敏锐感知细胞内ATP变化,几乎所有线粒体应激后都会迅速激活其调控作用。有研究表明,AMPK可以诱导线粒体自噬[7],AMPK/ULK1和AMPK/哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)都是调节线粒体自噬的重要通路[2,8]
细胞内能量状态的改变是触发AMPK激活的关键因素。正常生理状态下,细胞内ATP含量相对稳定,维持着细胞的各项代谢活动。当细胞面临营养物质缺乏、缺氧、运动耗能或能量生成受限等情况时,细胞内AMP/ATP比值会显著升高[9]。这种变化会被γ亚基敏锐感知,进而通过变构调节使得AMPK的活性构象发生改变[10],AMP的变构激活会导致完整细胞中乙酰辅酶A羧化酶的磷酸化增加,促进其磷酸化的同时抑制Thr172位点的去磷酸化[11],最终导致AMPK被激活。在动物机体内,AMP是激活AMPK的一个重要因素,另一方面也可以由肝激酶B1(LKB1)或者机体运动激活[1213]图1),AMPK能够通过多种途径激活PGC−1α的表达,还能够激活ULK1,进而激活自噬;同时也是mTOR的负调节剂,使其磷酸化失活,进而抑制蛋白合成等。但在某些细胞类型中是通过钙/钙调蛋白依赖性蛋白激酶2(CaMKK2或CaMKKβ)来增强其激酶活性[14]
线粒体自噬的概念由Lemasters等[16]提出,是细胞通过自噬机制选择性清除自身内部受损、老化或者功能异常线粒体的过程。在细胞的生命历程中,线粒体由于持续参与能量代谢以及不断受到内外环境因素的影响,不可避免地出现膜电位下降、活性氧(reactive oxygen species,ROS)生成过多、呼吸链功能障碍等损伤情况。如果这些受损线粒体不及时清除,会导致释放大量ROS以及凋亡因子[17],引发细胞内的氧化应激反应,甚至诱导细胞凋亡。线粒体自噬能够精准识别并清除损伤或失活的线粒体[18],维持细胞的功能完整性和内环境稳定,对于细胞的正常生理代谢活动以及动物机体健康有着不可或缺的作用。
泛素介导PINK1−Parkin是目前研究最为深入且经典的线粒体自噬调控通路,主要调节泛素依赖性线粒体自噬[19]。线粒体受损导致膜电位下降时,激活稳定在线粒体外膜上的PINK1 蛋白并发生自磷酸化,进而激活下游Parkin(一种E3泛素连接酶),来招募泛素(Ubiquitin, Ub)分子,催化其在受损线粒体蛋白上形成泛素链,启动线粒体自噬。磷酸化的泛素链被特定的自噬接头蛋白识别,与一系列蛋白复合物结合,通过其LC3相互作用区域与ATG8蛋白家族结合,从而将受损线粒体紧密连接到正在形成的自噬膜上。随着吞噬膜的延伸和扩展,其最终包裹受损线粒体,通过闭合形成完整的自噬体,随后与溶酶体融合,内容物被降解,完成线粒体的清除与成分回收。PINK1/Parkin介导线粒体自噬可挽救成骨细胞凋亡,促进骨形成[20]。线粒体自噬相关蛋白可以作为靶点,通过PINK1/Parkin通路调节线粒体裂变,诱导线粒体自噬,降解功能失调和支离破碎的线粒体(图2[2122]
除了PINK1/Parkin通路外,还有一些其他信号通路也参与线粒体自噬的调控。线粒体自噬受体蛋白BNIP3和NIX在细胞应对缺氧过程发挥着重要作用[23],可以直接与LC3结合,促进线粒体与自噬体的连接,启动线粒体自噬程序。FUNDC1作为一种定位于线粒体外膜的蛋白,在缺氧条件下其酪氨酸残基会发生去磷酸化,增强与LC3的相互作用,诱导线粒体自噬发生[24]
AMPK可通过直接MFF促进线粒体分裂。当AMPK对其进行磷酸化修饰后,能够增强MFF与动力相关蛋白1(Drp1)的相互作用,促进Drp1在线粒体上的募集,从而驱动线粒体发生分裂,形成较小的线粒体片段[4]。这些碎片化的线粒体更容易被自噬体识别并包裹,进而成为线粒体自噬的底物,为后续的自噬清除过程提供条件。通过药物激活肝脏细胞AMPK后,磷酸化水平显著升高,同时伴随着线粒体分裂现象的加剧以及线粒体自噬通量的增加[25]
激活TANK−binding kinase 1(TBK1)增强自噬体对线粒体的吞噬作用。TBK1是一种在自噬过程中发挥重要作用的激酶[26],AMPK激活后的TBK1能够磷酸化多个与自噬相关的蛋白,特别是那些参与自噬体形成以及自噬体与线粒体相互作用的蛋白,从而增强自噬体对线粒体的识别、包裹和吞噬能力,促进线粒体自噬的顺利进行。在脂肪细胞实验中激活AMPK后,可以通过由AMPK下游靶标ULK1介导的磷酸化来增加TBK1活性,调节营养过度和营养不良的能量传感[27],这表明AMPK可能通过TBK1对线粒体自噬起正向调控作用。
AMPK与自噬开端的激酶ULK1之间相关联。ULK1作为自噬起始过程中的核心调控因子,其激活后能够启动一系列自噬相关蛋白的组装和活化[28],促进自噬体的形成,进而为线粒体自噬的发生奠定基础。AMPK可以直接磷酸化ULK1的2个关键位点Ser556和Ser694,激活ULK1的激酶活性;ULK1还可以使自身分子结构发生改变,可以与14−3−3蛋白结合,使其无法被募集到线粒体上与受体NIX相互作用,抑制NIX依赖性线粒体自噬[5]。通过CRISPR技术建立的多西环素诱导ULK1基因激活的小鼠胚胎干细胞系显示[29],ULK1蛋白的磷酸化特征受AMPK和mTOR激酶调控,且ULK1的激活促进了自噬相关蛋白Beclin−1的积累,且AMPK/ULK1依赖的自噬对小鼠胚胎干细胞的多能性和自我更新有重要影响,通过维持mTOR/AMPK/ULK1途径的平衡,促进分解代谢过程以维持细胞的多能性。
过氧化物酶体增殖物激活受体γ共激活因子1α(PGC−1α)是线粒体生物合成的关键调节因子,在维持线粒体功能和数量方面具有重要作用。AMPK激活后能够通过多种途径上调PGC−1α的表达,一方面可以直接磷酸化PGC−1α,增强其转录活性[30];另一方面也可以通过调节一些转录因子的活性来间接促进PGC−1α的表达[31]。适量的PGC−1α表达增加能够驱动线粒体的生成和功能恢复,补充因线粒体自噬而被清除的线粒体,从而在细胞内建立起一种动态平衡[32],既保证了受损线粒体能够及时被清除[33],又能维持线粒体数量和功能满足细胞正常代谢的需求[34]
mTOR是细胞内重要的信号枢纽,同时也是自噬的关键负调控因子。AMPK可以磷酸化并抑制mTOR的活性,当AMPK被激活时,通过对mTOR的抑制,解除了mTOR对自噬过程的抑制作用,使得自噬相关蛋白能够正常发挥功能,促进线粒体自噬以及其他类型自噬的发生[35]。线粒体依赖性细胞凋亡和自噬、下丘脑线粒体介导的细胞凋亡通过AMPK/mTOR通路诱导[3637],谷胱甘肽过氧化物酶3也通过AMPK/mTOR途径抵抗线粒体自噬[38]
动物在养殖过程中常常面临各种应激因素,如营养缺乏、氧化应激、疾病感染、环境温度变化等,这些应激源对细胞内的能量代谢和线粒体功能产生不同程度的影响,AMPK与线粒体自噬之间会产生协同作用。
当动物面临食物短缺或者营养成分不均衡的情况时,细胞内能量供应急剧减少,AMP/ATP比值升高,激活AMPK信号通路[39]。AMPK的激活会启动上述提到的多种调控机制,促进线粒体自噬的发生,及时清除因缺乏营养物质而功能受损的线粒体,同时通过调节代谢途径,增强细胞对有限营养物质的摄取和利用效率,尽可能维持细胞的基本能量代谢需求,保障细胞在营养缺乏状态下的生存能力[40]。有研究证实[3],在能量应激下,AMPK通过MFF来促进线粒体分裂,而线粒体分裂是线粒体自噬的前提步骤。
在动物体内,由于各种内外源性因素(如毒素摄入、病原体感染等)会导致ROS生成过多,引发氧化应激反应,对线粒体造成氧化损伤,破坏其膜电位和呼吸链功能[41]。AMPK能够感知到细胞内能量代谢紊乱的情况而被激活,一方面通过促进线粒体自噬清除受损线粒体,减少ROS的进一步产生;另一方面AMPK还可以激活细胞内的抗氧化防御系统,如Nrf2信号通路,增强抗氧化酶(如超氧化物歧化酶、谷胱甘肽过氧化物酶等)的表达和活性,协同对抗氧化应激损伤,保护细胞的正常功能[42]。Guo等[43]研究发现,在奶牛乳腺炎发病过程中,乳腺细胞遭受氧化应激,AMPK信号通路被激活,诱导线粒体自噬,同时提高细胞内抗氧化能力,减轻炎症对乳腺组织的损伤,有助于维持奶牛的产奶性能和乳腺健康。
病原体感染动物后,除直接对细胞造成损伤外,还会扰乱细胞内的能量代谢平衡,导致线粒体功能障碍。AMPK在这种情况下会迅速做出响应,激活相关调控机制来诱导线粒体自噬,清除被病原体影响或者因免疫反应而受损的线粒体,避免过度的炎症反应和细胞凋亡[44]。AMPK还可以调节免疫细胞的代谢重编程,增强免疫细胞的杀菌和抗炎能力,帮助动物机体抵御疾病[45]。Chen等[46]发现,在猪感染猪瘟病毒后,脾脏细胞内AMPK活性增强,通过促进线粒体自噬维持免疫细胞的能量代谢和功能,破坏脂质代谢,增强机体的抗病毒能力,减轻猪瘟病毒对猪体健康的危害。
在动物肌肉发育过程中,线粒体自噬和AMPK也发挥着关键作用。适度的线粒体自噬有助于清除肌肉细胞中因运动、代谢产生损伤的线粒体,维持肌肉细胞的能量稳态,促进肌纤维的正常发育和成熟[32]。而AMPK通过调控线粒体自噬以及相关代谢通路,影响肌肉细胞内的糖原储备、脂肪含量以及蛋白质合成等,最终决定了肉质的嫩度、色泽、风味等品质指标[47]。通过特定的营养添加剂激活猪肌肉细胞中的AMPK信号通路,能够减少肌肉中脂肪的异常沉积,提高肌肉的保水性和嫩度,改善猪肉的品质,满足消费者对高品质肉类产品的需求[48]
动物机体面临氧化应激、疾病感染等应激情况时,AMPK与线粒体自噬通过协同作用,及时清除受损线粒体,减少ROS的产生,同时激活抗氧化防御系统,增强细胞和机体的抗氧化能力,减轻氧化应激对组织器官的损伤[49]。这种协同作用还能帮助动物更好地应对环境温度变化、运输应激等其他应激因素,维持机体的内环境稳定,提高动物的抗应激能力,保障动物在复杂养殖环境下的健康状态[5052]。在夏季高温环境下,家禽容易出现热应激反应,体内AMPK被激活,诱导线粒体自噬,能够通过增加肉鸡线粒体功能相关基因的表达,减少热应激对细胞线粒体的损伤,同时调节机体的散热机制和代谢状态,降低热应激对家禽生产性能和健康的影响[53]
AMPK与线粒体自噬在动物的免疫调节过程也至关重要。免疫细胞在执行免疫功能时消耗大量能量,线粒体作为能量供应的关键来源,其功能状态影响着免疫细胞的活性和功能发挥[54]。AMPK通过调控线粒体自噬,维持免疫细胞内线粒体的质量和功能,保障免疫细胞在应对病原体入侵时能够正常产生免疫应答,如激活T细胞、B细胞的增殖分化以及增强吞噬能力等[5557]。在疾病发生过程中,通过调节AMPK与线粒体自噬的平衡,还可以减轻炎症反应对组织的损伤,促进机体的康复。
尽管已有研究揭示了AMPK与线粒体自噬之间的相互作用,但具体的分子机制仍不完全清楚。未来还需要利用高通量测序、蛋白质组学等先进技术手段,进一步挖掘参与AMPK与线粒体自噬的蛋白和信号通路,以深入理解其相互作用的详细机制。在畜牧生产中,通过调控AMPK激活线粒体自噬,可能有助于改善动物的代谢状态,减少代谢性疾病的发生,提高动物的整体健康水平;通过促进线粒体自噬,还可以优化线粒体的功能和数量,进而提高饲料的利用率,降低生产成本;同时基于AMPK与线粒体自噬的相互作用,可以开发针对特定动物疾病或提高饲料利用率的新型饲料添加剂等。随着生物技术和研究方法的不断进步,未来将有更多先进的技术手段可用于AMPK与线粒体自噬的研究,这些技术手段将为揭示AMPK与线粒体自噬的详细分子机制、拓展应用领域以及探索其与动物健康的相互作用关系提供更多可能性。
  • 北京农学院人才强教工程项目(5066516008−6)
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2026年第44卷第11期
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doi: 10.3981/j.issn.1000-7857.2025.05.00019
  • 接收时间:2025-05-07
  • 首发时间:2026-06-23
  • 出版时间:2026-06-13
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  • 收稿日期:2025-05-07
  • 修回日期:2025-11-13
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北京农学院人才强教工程项目(5066516008−6)
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    1北京农学院动物科学技术学院,北京 102206
    2北京市农林科学院畜牧兽医研究所,北京 100097
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2种不同金属材料的力学参数

Family
属数
Number of
genus
种数
Number of
species
占总种数比例
Percentage of
total species (%)

Genus
种数
Number of
species
占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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