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第46卷第9期 王振涛，张凯妮，苏东明. 脂滴⁃线粒体接触点在肝脏代谢障碍与缺血再灌注损伤中的研究进展［J］.
2026年9月 南京医科大学学报（自然科学版），2026，46（9）：1383-1397 ·1391 ·

（续表1）
Key molecules/ Significance related to liver Main
Research topic Main research conclusion
phenomena disease references
Dual phase interac⁃ PLIN5 deficiency/ PLIN5 deficiency can reduce exposure，de⁃ It is indicated that the contact ［22-23，
tion of PLIN5 overexpression crease fatty acid oxidation，and exacerbate point is not unidirectional pro⁃ 28］
lipid deposition；however，overexpression of tection or unidirectional patho⁃
PLIN5 in some models can alleviate lipid per⁃ genicity，but exhibits stage⁃de⁃
oxidation，iron death，and inflammation pendent characteristics
Contact imbalance Fatty acid oxida⁃ When there is a mismatch between lipid It is an important mechanism ［6-7，29］
and lipotoxicity am⁃ tion disorder，lipid droplet mobilization and mitochondrial utili⁃ connection point for the pro⁃
plification peroxidation zation，free fatty acids，diacylglycerols，ce⁃ gression from steatosis to stea⁃
ramides，and lipid peroxidation products ac⁃ tohepatitis
cumulate，forming a vicious cycle
Contact imbalance mtROS，mtDNA， Mitochondrial damage and mtDNA leakage A mechanistic bridge connect⁃ ［23-25］
and inflammation NLRP3 can activate the NLRP3 inflammasome，trans⁃ ing“metabolic imbalance ⁃ in⁃
amplification lating metabolic stress into persistent liver in⁃ flammation amplification”has
flammation been established
Contact abnormali⁃ STING， hepatic Mitochondrial DNA/STING signaling not Supported abnormal contact ［19，26-
ties and fibrosis stellate cell activa⁃ only drives inflammation，but also promotes points connecting hepatocyte 27］
progression tion the activation of hepatic stellate cells and metabolic imbalance with liver
fibrotic reprogramming microenvironment remodeling
Protective adapta⁃ Lipid droplet for⁃ Moderate lipid droplet formation during ische⁃ Supported contact points to ［34-35］

tion during the mation，lipid se⁃ mia can buffer the toxicity of free fatty acids；lean towards the “metabolic
ischemic phase of questration， and lipolysis can reduce ROS，increase ATP，and buffering platform”during the
HIRI degreasing improve cell survival ische⁃mic phase
Injury amplifica⁃ Lipid droplet mo⁃ If there is a mismatch between lipid droplet It is an important mechanism ［30-36］
tion during HIRI bilization ⁃ mito⁃ mobilization and mitochondrial uptake/oxida⁃ node that explains why fatty
reperfusion period chondrial utiliza⁃ tion after reperfusion，the lipid droplets de⁃ liver is more prone to IRI
tion mismatch，rived from lipid droplets can be converted
cholesterol load into damage amplifiers，promoting ROS gen⁃
eration，mitochondrial depolarization，and an
increased tendency for mPTP opening
Aseptic inflamma⁃ mtDNA ⁃ cGAS ⁃ Mitochondrial damage releases mtDNA，acti⁃ Abnormal contact points not ［38-39］
tory pathway in STING vates cGAS STING，and amplifies aseptic only affect metabolism，but also
HIRI inflammation determine the leakage of dan⁃
ger signals
Emerging regulatory HSD17B13， BMAL1/HSD17B13 axis regulates HIRI diur⁃ The lipid droplet mitochondrial ［37，40］
networks in HIRI BMAL1，autopha⁃ nal differences by affecting autophagy flux contact point should be includ⁃
gy/lipolysis and lipid degradation ed in the higher⁃level regulatory
network of rhythm，autophagy，
and lipolysis

4.2 分离富集策略：从“漂浮的脂滴”到“界面相关 度离心。Brasaemle 和 Wolins的经典方案指出，脂滴
线粒体” 因密度高于大多数细胞器而易于上浮，但他们也特别
如果说成像技术回答的是“是否存在接触”的 强调：线粒体和内质网等膜结构常与脂滴紧密贴附，
问题，那么分离富集技术回答的则是“哪些分子位 因此完全获得脂滴组分而不被污染并不现实，这恰恰
［42］
于接触点”的问题。传统脂滴分离主要依赖密度梯 是脂滴接触位点研究的技术难点 。此后，Benador