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BACKGROUND: It has been found that mitochondrial function is abnormal in patients with chronic fatigue syndrome, and the administration of coenzymes can improve the symptoms. Warm acupuncture is one of the most important treatments for this disease, but its mechanism of action is unclear. OBJECTIVE: To investigate the effects of warm acupuncture on the phosphatase and tens in inducible kinase 1 (PINK1)/Parkin pathway in the skeletal muscle of rats with chronic fatigue syndrome. METHODS: After 3 days of adaptive feeding, 32 male Sprague-Dawley rats were randomly divided into normal control, model, warm acupuncture, and coenzyme Q groups with 8 rats in each group. The chronic fatigue syndrome model was established by multiple factors, including swimming exhaustion, chronic immobilization and fasting. After successful modeling, the normal group and the model group were treated with the same fixation and gavage procedures, and the warm acupuncture group was treated with acupuncture at Guanyuan, Zhongwan and Zusanli (bilateral) points, once a day. After the needling was inserted, the moxa pillar was put on the needle handle and ignited, three sessions once. The coenzyme Q group was given 1 mL/kg coenzyme by gavage, once a day for 14 days. The body mass, exhaustive swimming time and food utilization rate during the treatment were recorded. After the treatment, the bilateral gastrocnemius muscles of rats in each group were collected. The pathological morphology of the gastrocnemius muscle was observed by hematoxylin-eosin staining, the mitochondrial morphology and autophagosome of the gastrocnemius muscle were observed by transmission electron microscope. The expression level of microtubule-associated protein light chain 3 (LC3) II protein in the skeletal muscle was detected by immunohistochemistry. Western blot was used to detect the expression of PINK1, Parkin, LC3 I, and LC3 II in the skeletal muscle. RESULTS AND CONCLUSION: Compared with the normal group, the gastrocnemius muscle nuclei of the model group were pyknotic, condensed, the number of cells was increased, the cells were arranged disorderly, and the fibers in the gastrocnemius muscle were tightly arranged in the model group. Compared with the model group, the intercellular space became smaller, the nuclei were reduced, and the cell arrangement was orderly in the warm acupuncture group and coenzyme Q group. Compared with the normal group, the skeletal muscle mitochondria in the model group were swollen, fused, and vacuolated seriously, the membrane was partially broken, the matrix was more dissolved, the cristae was broken and disappeared, and autophagy appeared. Compared with the model group, the number of mitochondria increased, the arrangement was relatively neat, mitochondrial vacuolization and rupture of cristae in the gastrocnemius muscle were improved, the membrane structure was relatively intact, and autophagy occurred. Compared with the normal group, the expression of PINK1 protein in the skeletal muscle of the model group was significantly increased (P < 0.05), while the expression of Parkin, LC3 II and LC3 II/I protein was slightly upregulated (P > 0.05). Compared with the model group, the protein expressions of PINK1, Parkin, LC3 II and LC3 II/I were significantly upregulated in the warm acupuncture and coenzyme Q groups (P < 0.05), and the up-regulation was more significant in the warm acupuncture group. To conclude, warm acupuncture can play a role in the treatment of chronic fatigue syndrome by activating the PINK1/Parkin pathway, upregulating LC3 II expression, forming mitochondrial autophagosomes, promoting the degradation of damaged mitochondria, and improving mitochondrial quality. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of acacetin (Aca) on the proliferation, apoptosis and migration of liver cancer HepG2 cells by regulating PTEN induced kinase 1 (PINK1)/E3 ubiquitin protein ligase (Parkin) pathway mediated mitochondrial autophagy. Methods Liver cancer HepG2 cells were divided into the control group (normally cultured HepG2 cells), the Aca group (10 µmol/L Aca), the PINK1 small interfering RNA negative control (si-NC) group (transfected with si-NC), the PINK1 small interfering RNA (si-PINK1) group (transfected with si-PINK1), the Aca+si-NC group (treated with 10 µmol/L Aca after transfection of si-NC) and Aca+si-PINK1 group (treated with 10 µmol/L Aca after transfection of si-PINK1). Cell counting kit-8 (CCK-8) method was used to detect cell proliferation. Flow cytometry was used to detect cell apoptosis. Transwell test was used to detect cell migration. Transmission electron microscope was used to observe the formation of autophagosomes. Western blot assay was used to detect expression levels of autophagy related proteins [Beclin1, microtubule associated protein 1 light chain 3 (LC3)-Ⅰ and LC3-Ⅱ］and PINK1/Parkin pathway related proteins in cells. Results Compared with the control group, the survival rate and the number of migrating of HepG2 cells were significantly decreased in the Aca group, and the apoptosis rate, number of autophagy bodies, expression levels of Beclin-1, LC3-Ⅱ/LC3-Ⅰ, PINK1 and Parkin protein were increased significantly (P＜0.05). The survival rate and the number of migrating of HepG2 cells were significantly increased in the si-PINK1 group, and the apoptosis rate, number of autophagy bodies, expression levels of Beclin-1, LC3-Ⅱ/LC3-Ⅰ, PINK1 and Parkin protein were decreased significantly (P＜0.05). Compared with the Aca group and the Aca+si-NC group, the survival rate and the number of migrating of HepG2 cells were significantly increased in the Aca+si-PINK1 group, and the apoptosis rate, number of autophagy bodies, expression levels of Beclin-1, LC3- Ⅱ/LC3- Ⅰ, PINK1 and Parkin protein were decreased significantly (P＜0.05). Conclusion Aca may inhibit the proliferation and migration and promote cell apoptosis of liver cancer HepG2 cells by activating mitochondrial autophagy mediated by PINK1/Parkin pathway. [ABSTRACT FROM AUTHOR]

Objective This study aimed to explore the specific mechanism, mediated by the reactive oxygen species (ROS) and PINK1/Parkin pathway, of the mitochondrial autophagy of human periodontal ligament cells (hPDLCs) under starvation conditions. Methods hPDLCs were isolated and cultured from normal periodontal tissues. Earle's balanced salt solution (EBSS) was used to simulated a starvation environment and thus stimulate hPDLCs mitochondrial autophagy. N-Acetyl-L-cysteine (NAC) was used to inhibit ROS production to explore the role of ROS in hPDLC mitochondrial autophagy. Cyclosporin A was used to inhibit the PINK1/Parkin pathway to study the role of ROS and the PINK1/Parkin pathway in hPDLCs activation under starvation. The mitochondrial membrane potential was detected by flow cytometry with a JC-1 mitochondrial membrane potential detection kit. The morphological structure of mitochondria and the formation of mitochondrial autophagosome were observed by transmission electron microscopy. Mito tracker red cmxros and lyso tracker green staining were used to observe the localization of mitochondria and lysosomes. The formation intensity of ROS was detected with a DCFH-DA ROS fluorescent probe. The expression levels of mitochondrial autophagy genes (Tomm20 and Timm23) and the PINK1/Parkin pathway were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The expression levels of mitochondrial autophagy proteins (Tomm20 and Timm23) and PINK1/Parkin protein were detected by Western blot. Results EBSS starvation for 30 min induced the strongest activation of hPDLCs mitochondrial autophagy, increased the expression of ROS, downregulated the expression of mitochondrial autophagy-related genes (Tomm20 and Timm23) (P<0.001), and upregulated the PINK1/Parkin pathway (P<0.001). After NAC inhibited ROS production, mitochondrial autophagy was also inhibited. Meanwhile, the expression of Tomm20 and Timm23 was upregulated (P<0.001 and P<0.05), and the expression of the PINK1/parkin pathway (P<0.001 and P<0.05) was down regulated. When cyclosporin A inhibited the expression of the PINK1/Parkin pathway (P<0.05 and P<0.05), it reversed the mitochondrial autophagy of hPDLCs (P<0.001 and P<0.01) and also upregulated the expression of Tomm20 and Timm23 (P<0.001 and P<0.01). Conclusion ROS enhanced the mitochondrial autophagy of hPDLCs primarily through the PINK1/Parkin pathway under starvation conditions. [ABSTRACT FROM AUTHOR]

Objective To elucidate the ameliorative effect of AP39 on myocardial fibrosis in uremic rats and investigate its possible mechanism. Methods Forty SD male rats were randomly and equally divided into 4 groups: Sham group, uremic cardiomyopathy group (UCM group), AP39 intervention group (UCM+AP39 group) and AP39 control group (n=10). The rats in the UCM group and the UCM+AP39 group were treated with classical operation of 5/6 nephrectomy to establish the uremic cardiomyopathy model, and then the rats in the latter 2 groups were given intraperitoneal injection of AP39 (100 nmol/kg, once a day) for 4 weeks, while those of the Sham and model groups were intraperitoneally injected with the same amount of normal saline. Ultrasonic imaging platform was used to detect the value of left ventricular fractional shortening (LVFS) of rats in each group. Masson staining and immunohistochemical staining were performed respectively to observe collagen deposition and the expression of Collagen Ⅲ protein in the myocardial interstitial tissue of each group. Western blotting was adopted to determine the expression levels of PETN-induced putative kinase-1 (PINK1), Parkinson's disease protein (Parkin), autophagy-related gene-5 (Atg5), microtubule-associated protein-1 light chain-3 Ⅱ/Ⅰ(LCEⅡ/Ⅰ), Beclin1 and P62 (also called sequestosome, SQSTM1) in the myocardial tissue of each group. Results As compared with those in the Sham group, the rats in the UCM group had significantly decreased LVFS, increased collagen deposition content and Collagen Ⅲ protein level (P < 0.05), and disordered arrangement in myocardial tissue. The expression levels of PINK1, Parkin, Atg5, LC3Ⅱ/Ⅰand Beclin1 were significantly reduced, while the level of P62 was enhanced in the UCM group (P < 0.05). By contrast, the rats in the UCM+AP39 group had higher LVFS, lower collagen deposition content and Collagen Ⅲ protein level than those in the UCM group (P < 0.05), the expression levels of PINK1, Parkin, Atg5, LC3 Ⅱ/Ⅰ and Beclin1 were remarkably up-regulated, and the level of P62 down-regulated (P < 0.05). Conclusion AP39 can improve uremic myocardial fibrosis in rats, which may be related to the up-regulation of PINK1/Parkin-mediated mitophagy.

This study explored the effect of Tianma Gouteng Decoction on oxidative stress induced by angiotensin Ⅱ(AngⅡ) in vascular smooth muscle cell(VSMC) and its molecular mechanism. Primary rat VSMC were cultured using tissue block method, and VSMC were identified by α-actin immunofluorescence staining. AngⅡ at a concentration of 1×10~(-6) mol·L~(-1) was used as the stimulating factor, and Sprague Dawley(SD) rats were orally administered with Tianma Gouteng Decoction to prepare drug serum. Rat VSMC were divided into normal group, model group, Chinese medicine group, and inhibitor(3-methyladenine, 3-MA) group. Cell counting kit-8(CCK-8) assay was used to detect cell proliferation activity. Bromodeoxyuridine(BrdU) flow cytometry was used to detect cell cycle. Transwell assay was used to detect cell migration ability. Enzyme-linked immunosorbent assay(ELISA) was used to detect the activity of superoxide dismutase(SOD), catalase(CAT), and malondialdehyde(MDA) in VSMC. The intracellular reactive oxygen species(ROS) fluorescence intensity was detected using DCFH-DA fluorescent probe. Western blot was used to detect the expression of PTEN-induced putative kinase 1(PINK1), Parkin, p62, and microtubule-associated protein 1A/1B-light chain 3(LC3-Ⅱ) proteins in VSMC. The results showed that Tianma Gouteng Decoction-containing serum at a concentration of 8% could significantly inhibit VSMC growth after 48 hours of intervention. Compared with the normal group, the model group showed significantly increased cell proliferation activity and migration, significantly decreased levels of SOD and CAT, significantly increased levels of MDA, significantly enhanced ROS fluorescence intensity, significantly decreased expression of PINK1, Parkin, and LC3-Ⅱ proteins, and significantly increased expression of p62 protein. Compared with the model group, the Chinese medicine group showed significantly reduced cell proliferation activity and migration, significantly increased levels of SOD and CAT, significantly decreased levels of MDA, significantly weakened ROS fluorescence intensity, significantly increased expression of PINK1, Parkin, and LC3-Ⅱ proteins, and significantly decreased expression of p62 protein. Compared with the Chinese medicine group, the addition of the mitochondrial autophagy inhibitor 3-MA could block the intervention of Tianma Gouteng Decoction-containing serum on VSMC proliferation, migration, mitochondrial autophagy, and oxidative stress levels, with statistically significant differences. In summary, Tianma Gouteng Decoction has good antioxidant activity and can inhibit cell proliferation and migration. Its mechanism of action may be related to the activation of the mitochondrial autophagy PINK1/Parkin signaling pathway.

[Objectives] The aim of this study was to investigate the effects of decabromodiphenyl ether(BDE-209) exposed to broilers on kidney damage,and to explore the potential nephrotoxicity and mechanisms. [Methods] One day-old 150 male AA broilers were randomly allotted to 5 groups with 6 replicates per group and 5 broilers per replicate. The broilers were exposed to BDE-209 concentrations with 0,0.004,0.04,0.4,4.0 g·kg-1 added to a standard diet for 42 days,respectively. At the end of the experiment,the concentration of blood urea nitrogen(BUN) and creatinine(CRE) in serum as well as kidney oxidative stress indexes were measured,and the histological and morphological structure and mitochondrial membrane potential of kidney were observed. The expression of autophagy proteins involving in p62,microtubule-associated protein 1 light chain 3(LC3) and PTEN-inducible kinase 1(PINK1)/Parkin signaling pathway were analyzed by fluorescence immunohistochemistry,real-time PCR and western blot. [Results] Compared with control,kidney injury was observed at different BDE-209 treatment groups,including glomerular enlargement and cellular composition increased,renal tubular edema and cytoplasmic porosity and mitochondrial membrane potential decreased in kidney. Additionally,the levels of BUN,CRE in serum increased significantly(P<0.05) when the content of BDE-209 was upper 0.04 g·kg-1,and the activities of SOD and GSH-Px in 0.4 and 4.0 g·kg-1 BDE-209 groups decreased significantly(P<0.05),the concentration of MDA increased in 0.04,0.4 and 4.0 g·kg-1 BDE-209 groups(P<0.05). Moreover,the expression level of p62 and the ratio of LC3-â…¡/LC3-â…  increased(P<0.05),and the PINK1 expression were also significantly up-regulated in kidney tissues(P<0.05). [Conclusions] BDE-209 exposure can cause kidney damage,and the underlying mechanisms may be that BDE-209 exacerbate oxidative stress,then activate PINK1/Parkin pathway to induce mitochondrial injury,promote the transformation of autophagy protein LC3-â…  to LC3-â…¡ and the accumulation of p62 protein,which hindere the degradation of autophagy and resulted in the renal injury. 参考文献/References: [Objectives] The aim of this study was to investigate the effects of decabromodiphenyl ether(BDE-209) exposed to broilers on kidney damage,and to explore the potential nephrotoxicity and mechanisms. [Methods] One day-old 150 male AA broilers were randomly allotted to 5 groups with 6 replicates per group and 5 broilers per replicate. The broilers were exposed to BDE-209 concentrations with 0,0.004,0.04,0.4,4.0 g·kg-1 added to a standard diet for 42 days,respectively. At the end of the experiment,the concentration of blood urea nitrogen(BUN) and creatinine(CRE) in serum as well as kidney oxidative stress indexes were measured,and the histological and morphological structure and mitochondrial membrane potential of kidney were observed. The expression of autophagy proteins involving in p62,microtubule-associated protein 1 light chain 3(LC3) and PTEN-inducible kinase 1(PINK1)/Parkin signaling pathway were analyzed by fluorescence immunohistochemistry,real-time PCR and western blot. [Results] Compared with control,kidney injury was observed at different BDE-209 treatment groups,including glomerular enlargement and cellular composition increased,renal tubular edema and cytoplasmic porosity and mitochondrial membrane potential decreased in kidney. Additionally,the levels of BUN,CRE in serum increased significantly(P<0.05) when the content of BDE-209 was upper 0.04 g·kg-1,and the activities of SOD and GSH-Px in 0.4 and 4.0 g·kg-1 BDE-209 groups decreased significantly(P<0.05),the concentration of MDA increased in 0.04,0.4 and 4.0 g·kg-1 BDE-209 groups(P<0.05). Moreover,the expression level of p62 and the ratio of LC3-Ⅱ/LC3-Ⅰ increased(P<0.05),and the PINK1 expression were also significantly up-regulated in kidney tissues(P<0.05). [Conclusions] BDE-209 exposure can cause kidney damage,and the underlying mechanisms may be that BDE-209 exacerbate oxidative stress,then activate PINK1/Parkin pathway to induce mitochondrial injury,promote the transformation of autophagy protein LC3-Ⅰ to LC3-Ⅱ and the accumulation of p62 protein,which hindere the degradation of autophagy and resulted in the renal injury. 参考文献/References: [ABSTRACT FROM AUTHOR]

BACKGROUND: In addition to FUNDC1, Bnip3 and Nix mitochondrial autophagy pathways in mammals that are closely related to the hypoxic environment, Pink1/Parkin is the main mitochondrial autophagy pathway after brain injury. PINK1 acts upstream of Parkin, and the Pink1/Parkin pathway is used to mediate loss of mitochondrial surface functional proteins or structural polyubiquitination, and considered as a marker for autophagosome selection, which has an important influence on autophagy-dependent degradation of depolarized mitochondria. OBJECTIVE: To analyze the role of Pink1/Parkin-mediated mitochondrial autophagy in rats with brain injury after hypertensive intracerebral hemorrhage. METHODS: The study was approved by the Laboratory Animal Ethical Committee of North Sichuan Medical College. Forty-five male Wistar rats of SPF grade were randomly divided into normal, model and autophagy inhibitor groups. The rats in the model and autophagy inhibitor groups were used to prepare hypertensive cerebral hemorrhage model. Before modeling 2 μL of PBS solution containing trimethyl adenine (100 nmoi/L) was intraperitoneally injected in the inhibitor group, and the model and the normal groups were intraperitoneally injected with 2 μL of PBS. The water content, mnochondnal autophagy, mnochondrial membrane potential, cerebral infarction, mitochondrial LC3, Parkin protein and PINK1 protein expression in brain tissue were detected. RESULTS AND CONCLUSION: (1) Compared with the normal group, the autophagy staining and mitochondrial staining expression in the model group was increased, and the number of co-localized positive cells was increased (both P < 0.05). Compared with the model group, the autophagy staining and mitochondrial staining expression in the autophagy inhibitor group was decreased, and the number of co-localized positive cells was decreased (both P < 0.05}. (2) Compared with the normal group, the infarction proportion of the brain in the model group was increased (P < 0.05). Compared with the model group, the infarction proportion of the brain in the autophagy inhibitor group was increased (P < 0.05). (3) Compared with the normal group, the mitochondrial staining intensity in the model group was decreased, and the autophagy staining intensity was increased (both P < 0.05). Compared with the model group, the mitochondrial staining intensity in the autophagy inhibitor group was decreased, and the autophagy staining intensity was increased (both P < 0.05). (4) Compared with the normal group, the expression levels of PINK1, LC3 and Parkin in the model group were increased (P < 0.05). Compared with the model group, the expression levels of PINK1, LC3 and Parkin in the autophagy inhibitor group were decreased (P < 0.05). In summary, mitochondrial autophagy can alleviate the degree of brain injury after hypertensive intracerebral hemorrhage. The Pink1/Parkin pathway plays an important role in the mitochondrial autophagy. [ABSTRACT FROM AUTHOR]

Mitophagy is the process of selective clearance of damaged mitochondria by autophagy. There are several regulatory mechanisms for mitophagy, and the PINK1/Parkin pathway is considered the main pathway for mitophagy. Recent studies have shown that PINK1/Parkin-mediated mitophagy plays an important role in the pathogenesis of various diseases including Parkinson’s disease. This article introduces the mechanism of PINK1/Parkin-mediated mitophagy and its role in various liver diseases including nonalcoholic fatty liver disease, liver fibrosis, and hepatocellular carcinoma, in order to provide new clues and ideas for the treatment of diseases. [ABSTRACT FROM AUTHOR]

Objective: To observe the effect of acupotomy on mitophagy mediated by PINK1/Parkin pathway in cartilage of rabbits with knee osteoarthritis (KOA), so as to explore its mechanism in inhibiting cartilage damage., Methods: Twenty-one New Zealand rabbits were randomly divided into normal, model, and acupotomy groups, with 7 rabbits in each group. The KOA rabbit model was established by using the Videman method. Rabbits in the acupotomy group received regular acupotomy treatment around the knee joint nodules or tendons once a week for 3 consecutive weeks. HE staining and transmission electron microscopy were used to observe the morphological and ultrastructural changes in knee joint cartilage of rabbits. Flow cytometry was used to measure the mitochondrial membrane potential (Δψm) and reactive oxygen species (ROS) average fluorescence intensity in chondrocytes. Immunofluorescence was performed to detect the fluorescence intensity of LC3B, PINK1 and Parkin in cartilage tissue. Western blot was conducted to measure the protein expression levels of p62, LC3Ⅱ/Ⅰ, PINK1, and Parkin in cartilage tissue., Results: Compared to the normal group, the model group showed fissures and tissue fibrosis on the surface of rabbit knee joint cartilages, loose distribution of chondrocytes, decreased autophagosomes, and abnormal mitochondrial morphology. The fluorescence intensity of LC3B, PINK1 and Parkin, the expression levels of LC3Ⅱ/Ⅰ, PINK1 and Parkin proteins in cartilage tissue were significantly decreased ( P <0.01), while the percentage of chondrocytes with low Δψm, the average fluorescence intensity of ROS, and the expression of p62 protein in cartilage tissue were significantly increased ( P <0.01). Compared to the model group, the acupotomy group showed no obvious defects on the surface of rabbit knee joint cartilage, relatively dense distribution of chondrocytes, increased autophagosomes, and relatively normal mitochondrial morphology. The fluorescence intensity of LC3B, PINK1 and Parkin, the expression of LC3Ⅱ/Ⅰ, PINK1 and Parkin proteins in cartilage tissue were significantly increased ( P <0.01, P <0.05), while the percentage of chondrocytes with low Δψm, the average fluorescence intensity of ROS, and the expression of p62 protein in cartilage tissue were significantly decreased ( P <0.01)., Conclusion: Acupotomy may promote mitophagy by regulating the PINK1/Parkin pathway, thereby improving cartilage damage in rabbits with KOA.

Objectives: This study aimed to explore the specific mechanism, mediated by the reactive oxygen species (ROS) and PINK1/Parkin pathway, of the mitochondrial autophagy of human periodontal ligament cells (hPDLCs) under starvation conditions., Methods: hPDLCs were isolated and cultured from normal periodontal tissues. Earle's balanced salt solution (EBSS) was used to simulated a starvation environment and thus stimulate hPDLCs mitochondrial autophagy. N-Acetyl-L-cysteine (NAC) was used to inhibit ROS production to explore the role of ROS in hPDLC mitochondrial autophagy. Cyclosporin A was used to inhibit the PINK1/Parkin pathway to study the role of ROS and the PINK1/Parkin pathway in hPDLCs activation under starvation. The mitochondrial membrane potential was detected by flow cytometry with a JC-1 mitochondrial membrane potential detection kit. The morphological structure of mitochondria and the formation of mitochondrial autophagosome were observed by transmission electron microscopy. Mito tracker red cmxros and lyso tracker green staining were used to observe the localization of mitochondria and lysosomes. The formation intensity of ROS was detected with a DCFH-DA ROS fluorescent probe. The expression levels of mitochondrial autophagy genes (Tomm20 and Timm23) and the PINK1/Parkin pathway were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The expression levels of mitochondrial autophagy proteins (Tomm20 and Timm23) and PINK1/Parkin protein were detected by Western blot., Results: EBSS starvation for 30 min induced the strongest activation of hPDLCs mitochondrial autophagy, increased the expression of ROS, downregulated the expression of mitochondrial autophagy-related genes (Tomm20 and Timm23) ( P <0.001), and upregulated the PINK1/Parkin pathway ( P <0.001). After NACinhibited ROS production, mitochondrial autophagy was also inhibited. Meanwhile, the expression of Tomm20 and Timm23 was upregulated ( P <0.001 and P <0.05), and the expression of the PINK1/parkin pathway ( P <0.001 and P <0.05) was down regulated. When cyclosporin A inhibited the expression of the PINK1/Parkin pathway ( P <0.05 and P <0.05), it reversed the mitochondrial autophagy of hPDLCs ( P <0.001 and P <0.01) and also upregulated the expression of Tomm20 and Timm23 ( P <0.001 and P <0.01)., Conclusions: ROS enhanced the mitochondrial autophagy of hPDLCs primarily through the PINK1/Parkin pathway under starvation conditions.