The key role of muscle spindles in the pathogenesis of myofascial trigger points according to ramp-and-hold stretch and drug intervention in a rat model.

This study investigated whether abnormal peak inversion spontaneous potentials (PISPs) recorded at resting myofascial trigger points (MTrPs) stem from the discharge of muscle spindles. Forty-eight male Sprague-Dawley rats were randomly divided into six groups. Five groups underwent MTrP modeling intervention, whereas one group did not receive intervention and was duly designated as the blank control. After model construction, five rat models were randomly subjected to ramp-and-hold stretch tests, succinylcholine injection, eperisone hydrochloride injection, saline injection, and blank drug intervention. By contrast, the rats in the blank control group were subjected to ramp-and-hold stretch tests as a control. Frequencies and amplitudes of PISPs were recorded pre- and post-interventions and compared with those of the blank group. Stretch tests showed that the depolarization time and amplitude of PISPs ranged from 0.4 ms to 0.9 ms and from 80 uV to 140 µV, respectively. However, no PISPs were observed in the control rats. The frequency of PISPs in the ramp and hold phases and the first second after the hold phase was higher than that before stretching (p < 0.01). Succinylcholine and eperisone exerted excitatory and inhibitory effects on PISPs, respectively. In the group injected with 0.9% saline, no considerable differences of the PISPs were observed during the entire observation period. In conclusion, PISPs recorded at resting MTrPs are closely related to muscle spindles. The formation of MTrPs may be an important factor that regulate dysfunctional muscle spindles.

YAP1-activated ZNF131 promotes hepatocellular carcinoma cell proliferation through transcriptional regulation of PAIP1.

Zinc finger protein 131 (ZNF131), a member of BTB-ZF transcription factors, has been previously reported as an oncogene in several human cancers. However, the function and underlying mechanism of ZNF131 in hepatocellular carcinoma (HCC) are still unclear. In our study, the upregulated expression of ZNF131 mRNA was confirmed in HCC tissues by analyzing the TCGA and GEO datasets. The immunohistochemical staining data also revealed the overexpression of ZNF131 protein in HCC samples. High expression of ZNF131 predicted poor overall survival and disease-free survival in HCC patients. ZNF131 knockdown inhibited the proliferation and colony formation and led to G2/M phase arrest of HCC cells, while its overexpression promoted HCC cell proliferation, cell cycle progression and colony formation. Moreover, ZNF131 silencing repressed the growth of HCC cells in nude mice. Yes-associated protein 1 (YAP1) was recognized as an upstream regulator of ZNF131. Both YAP1 knockdown and inactivation reduced ZNF131 expression in HCC cells, and YAP1 overexpression enhanced ZNF131 level. Interestingly, we found that poly(A) binding protein interacting protein 1 (PAIP1) was a novel target of ZNF131. ZNF131 silencing downregulated while ZNF131 overexpression upregulated PAIP1 expression in HCC cells. The luciferase reporter assay demonstrated that ZNF131 regulated PAIP1 expression at the transcription level. Notably, we revealed that ZNF131 activated the AKT signaling by enhancing PAIP1 expression in HCC cells. AKT inhibitor markedly attenuated ZNF131-enhanced HCC cell proliferation. Restoring PAIP1 expression abrogated the inhibitory effects of ZNF131 knockdown on HCC cell proliferation and colony formation. To conclude, ZNF131 was highly expressed and acted as an oncogene in HCC. ZNF131, which was activated by YAP1, promoted HCC cell proliferation through transcriptional regulation of PAIP1.

In vitro culture of muscle cells derived from myofascial trigger points.

OBJECTIVE: To examine for the in vitro existence of contractile nodules on the taut band of muscle fibers where myofascial trigger points (MTrPs) are located (using cell culture). METHODS: Sixteen male Sprague-Dawley rats (7 weeks old) were randomly divided into experimental and control groups. A blunt striking injury and eccentric exercise were applied to the gastrocnemius muscle of rats in the experimental group once a week for 8 weeks to establish an MTrP model. Subsequently, the rats were reared normally and rested for 4 weeks. After modeling, the skeletal muscles at the MTrPs (and non-MTrPs at the same anatomical position) were extracted from the two groups of rats for in vitro cell culture experiments of single muscle fibers. Potential contractile nodules in the MTrP group were exposed to different concentrations of acetylcholinesterase, whereas non-MTrP cells were exposed to acetylcholine. The morphological changes of muscle cells in each group were observed. RESULTS: By culturing MTrP cells in vitro, large contractile nodules remained in single MTrP muscle fibers, whereas some contractile nodules were twisted and deformed. After the addition of different acetylcholinesterase concentrations, no obvious morphological changes were observed in the contractile nodules in the MTrP group. After the non-MTrP cells were exposed to different acetylcholine concentrations, no significant morphological changes were observed in the single muscle fibers. CONCLUSION: MTrP cells can continue to maintain contractile morphology in vitro, but whether the recovery of such contractile nodules is related to acetylcholine remains uncertain.

Clinical observations in treatment of lower extremity varicose veins with trigger points acupuncture.

OBJECTIVES: To observe the effect of the acupuncture of myofascial trigger points (MTrPs) in the treatment of lower extremity varicose veins (LEVVs). METHODS: Overall, 260 patients with LEVVs participated in this study. LEVVs were selected based on diagnostic criteria of Clinical, Etiology, Anatomy, and Pathophysiology levels 2-5 and classified into six types on the basis of their anatomical positions. The MTrPs in the lower extremities were localized in accordance with the classification of LEVVs and treated by MTrPs acupuncture combined with self-massage and self-stretching. The interval between each treatment was 2 weeks to 1 month, depending on needling pain tolerance of each patient. An in-house evaluation was used to estimate the proportion of varicose veins in the lower limbs and their accompanying symptoms. The treatment effect was evaluated before each treatment and at 1-year follow-up. RESULTS: The mean evaluation score of LEVVs before the treatment course was 3.66 ± 1.19. After the course, this reduced to 1.18 ± 0.97, with the following response rates: 85% for excellent and good and 15% for medium. After 1-year follow-up, the mean evaluation score of all patients was 1.11 ± 0.92, with the following response rates: 87% for excellent and good, and 13% for medium. CONCLUSIONS: In some patients, MTrP acupuncture could cure LEVVs and its accompanying symptoms. These LEVVs are probably caused by fascia tension as a pre-pathology induced by the MTrPs.

FOXC2-AS1/FOXC2 axis mediates matrix stiffness-induced trans-differentiation of hepatic stellate cells into fibrosis-promoting myofibroblasts.

Matrix stiffness is a central modulator of hepatic stellate cells (HSCs) activation and hepatic fibrogenesis. However, the long non-coding RNAs (lncRNAs)-regulated transcriptional factors linking matrix stiffness to alterations in HSCs phenotype are not completely understood. In this study, we investigated the effects of matrix stiffness on HSCs activation and its potential mechanism. Through analysis the RNA-seq data with human primary HSCs cultured on 0.4 kPa and 25.6 kPa hydrogel, we identified that forkhead box protein C2 (FOXC2) and its antisense lncRNA FXOC2-AS1 as the new mechanosensing transcriptional regulators that coordinate HSCs responses to the matrix stiffness, moreover, FOXC2 and FOXC2-AS1 expression were also elevated in human fibrosis and cirrhosis tissues. The matrix stiffness was sufficient to activate HSCs into myofibroblasts, resulting in nuclear accumulation of FOXC2. Disrupting FOXC2 and FOXC2-AS1 level abrogated stiffness-induced activation of HSCs. Further mechanistic studies displayed that stiffness-upregulated lncRNA FOXC2-AS1 had no influence on transcription of FOXC2. FOXC2-AS1 exerted its biological function through maintaining the RNA stability of FOXC2, and protecting FOXC2 mRNA from degradation by RNA exosome complex. Additionally, rescue assays confirmed that reintroduction of FOXC2 in FOXC2-AS1-depleted HSCs reversed the repression of FOXC2-AS1 knockdown on stiffness-induced HSCs activation. In AAV6-treated mice fibrotic models, targeting FOXC2 in vivo lead to a reduced degree of liver fibrosis. In sum, our study uncovers a reciprocal crosstalk between matrix stiffness and FOXC2-AS1/FOXC2 axis leading to modulation of HSCs mechanoactivation and liver fibrosis, and present AAV6 shRNA as an effective strategy that targets FOXC2 leading to the resolution of liver fibrosis.

METTL3-induced lncRNA GBAP1 promotes hepatocellular carcinoma progression by activating BMP/SMAD pathway.

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common and challenging cancers in the world. N6-methyladenosine (m6A) modification and long non-coding RNAs (lncRNAs) play critical roles in the progression of HCC. However, there are few reports on genome-wide screening and functional annotations of m6A-methylated lncRNAs in HCC. METHODS: The expression levels of m6A methyltransferase METTL3 and the association with the prognosis in HCC were determined by RT-qPCR, public dataset platforms. Then, RNA-seq, Pearson correlation analysis, MeRIP-qPCR, RNA half-life assay, gene site-directed mutation, RIP assay and RT-qPCR analysis were employed to determine the downstream target of METTL3 in HCC. Subsequently, the expression levels and roles of lncRNA glucosylceramidase beta pseudogene 1 (GBAP1) in HCC were determined by Kaplan-meier curves, RT-qPCR, in vitro functional experiments and in vivo tumorigenesis and lung metastasis models. Then, the downstream target and pathway of GBAP1 were explored by GO biological process, KEGG pathway enrichment, luciferase reporter assay, RIP assay and rescue experiments and so on. RESULTS: METTL3 was upregulated in HCC and closely related to HCC prognosis. And METTL3 induced GBAP1 expression by acting as the m6A writer of GBAP1 and IGF2BP2 worked as its m6A reader. Clinically, GBAP1 expression was significantly associated with tumor size, venous infiltration, TNM stage and prognosis of HCC, Functionally, GBAP1 promoted HCC metastasis and growth both in vitro and in vivo. Furthermore, GBAP1 acted as the molecular sponge for miR-22-3p to increase the expression of bone morphogenetic protein receptor type 1A (BMPR1A), which then activated BMP/SMAD pathway in HCC cells. CONCLUSIONS: Our findings demonstrated that METTL3-induced GBAP1 promoted migration, invasion and proliferation of HCC cells via GBAP1/miR-22-3p/BMPR1A/SMAD axis. GBAP1 could be a potential prognosis indicator and therapeutic target for HCC.

A novel nomogram predicting the early recurrence of hepatocellular carcinoma patients after R0 resection.

Background: Early tumor recurrence is one of the most significant poor prognostic factors for patients with HCC after R0 resection. The aim of this study is to identify risk factors of early recurrence, in addition, to develop a nomogram model predicting early recurrence of HCC patients. Methods: A total of 481 HCC patients after R0 resection were enrolled and divided into a training cohort (n = 337) and a validation cohort (n = 144). Risk factors for early recurrence were determined based on Cox regression analysis in the training cohort. A nomogram incorporating independent risk predictors was established and validated. Results: Early recurrence occurred in 37.8% of the 481 patients who underwent curative liver resection of HCC. AFP ≥ 400 ng/mL (HR: 1.662; P = 0.008), VEGF-A among 127.8 to 240.3 pg/mL (HR: 1.781, P = 0.012), VEGF-A > 240.3 pg/mL (HR: 2.552, P < 0.001), M1 subgroup of MVI (HR: 2.221, P = 0.002), M2 subgroup of MVI (HR: 3.120, P < 0.001), intratumor necrosis (HR: 1.666, P = 0.011), surgical margin among 5.0 to 10.0 mm (HR: 1.601, P = 0.043) and surgical margin < 5.0 mm (HR: 1.790, P = 0.012) were found to be independent risk factors for recurrence-free survival in the training cohort and were used for constructing the nomogram. The nomogram indicated good predictive performance with an AUC of 0.781 (95% CI: 0.729-0.832) and 0.808 (95% CI: 0.731-0.886) in the training and validation cohorts, respectively. Conclusions: Elevated serum concentrations of AFP and VEGF-A, microvascular invasion, intratumor necrosis, surgical margin were independent risk factors of early intrahepatic recurrence. A reliable nomogram model which incorporated blood biomarkers and pathological variables was established and validated. The nomogram achieved desirable effectiveness in predicting early recurrence in HCC patients.

HIF-1α-activated TMEM237 promotes hepatocellular carcinoma progression via the NPHP1/Pyk2/ERK pathway.

BACKGROUND: Hypoxia-inducible factors (HIFs) are the most essential endogenous transcription factors in the hypoxic microenvironment and regulate multiple genes involved in the proliferation, migration, invasion, and EMT of hepatocellular carcinoma (HCC) cells. However, the regulatory mechanism of HIFs in driving HCC progression remains poorly understood. METHODS: Gain- and loss-of-function experiments were carried out to investigate the role of TMEM237 in vitro and in vivo. The molecular mechanisms involved in HIF-1α-induced TMEM237 expression and TMEM237-mediated enhancement of HCC progression were confirmed by luciferase reporter, ChIP, IP-MS and Co-IP assays. RESULTS: TMEM237 was identified as a novel hypoxia-responsive gene in HCC. HIF-1α directly bound to the promoter of TMEM237 to transactivate its expression. The overexpression of TMEM237 was frequently detected in HCC and associated with poor clinical outcomes in patients. TMEM237 facilitated the proliferation, migration, invasion, and EMT of HCC cells and promoted tumor growth and metastasis in mice. TMEM237 interacted with NPHP1 and strengthened the interaction between NPHP1 and Pyk2 to trigger the phosphorylation of Pyk2 and ERK1/2, thereby contributing to HCC progression. The TMEM237/NPHP1 axis mediates hypoxia-induced activation of the Pyk2/ERK1/2 pathway in HCC cells. CONCLUSIONS: Our study demonstrated that HIF-1α-activated TMEM237 interacted with NPHP1 to activate the Pyk2/ERK pathway, thereby promoting HCC progression.

Novel Synthesis of Dihydroisoxazoles by p-TsOH-Participated 1,3-Dipolar Cycloaddition of Dipolarophiles withα-Nitroketones.

This article reports in detail a method for the synthesis of 3-benzoxoxazoline by the reaction of alkenes (alkynes) and a variety of α-nitroketones in the presence of p-TsOH. The scope of alkenes is broad, including different alkenes and the alkyne. This reaction provides a convenient and efficient synthetic method of 3-benzoylisoxazolines.

Patellofemoral Pain, Q-Angle, and Performance in Female Chinese Collegiate Soccer Players.

Background and objective: Female sports injuries have been neglected by science, and few relevant studies have considered female subjects. Knee pain in female soccer players is more common than in male soccer players. The number of days of absence from training and competition has been shown to be higher in females than males. The reporting of knee pain is common in female soccer players, but whether knee pain is associated with morphological features is unclear. The Q-angle of the knee has been hypothesized to be a causal factor in knee pain. Asian females have shown higher levels of valgus than non-sporting Caucasian populations, but no data exist for female Chinese players. The aim of our study was to investigate whether there are associations between knee pain, the Q-angle of the lower limb, jump performance, play time, and perceived exertion in female Chinese collegiate soccer players. Materials and Methods: We measured the Q-angle, patellofemoral/anterior knee pain (SNAPPS questionnaire), and CMJ and SJ performance of 21 subjects (age: 20.09 ± 1.13 years, weight: 56.9 ± 6.26 kg, height: 164.24 ± 4.48 cm, and >10 years of practice) before and after a match; Borg scale and play time results were also recorded. Results: We found that our studied group had higher Q-angles in comparison to other ethnic groups reported in the literature, as well as an association of the Q-angle with the age, height, and weight of the players; however, contrary to other studies, we did not find any association between the Q-angle and knee pain, jumps, play time, or perceived exertion. Knee pain was not associated with any of the measured variables. Conclusions: Female Chinese soccer players showed higher Q-angles than players of other ethnic groups, a result that was associated with anthropometrics. The Q-angle was not found to be associated with knee pain, for which the sole determinant was body height.

Hypoxia-induced lncRNA MRVI1-AS1 accelerates hepatocellular carcinoma progression by recruiting RNA-binding protein CELF2 to stabilize SKA1 mRNA.

BACKGROUND: Long non-coding RNAs (lncRNAs) perform a vital role during the progression of hepatocellular carcinoma (HCC). Here, we aimed to identify a novel lncRNA involved in HCC development and elucidate the underlying molecular mechanism. METHODS: The RT-qPCR and TCGA dataset analysis were applied to explore the expressions of MRVI1-AS1 in HCC tissues and cell lines. Statistical analysis was applied to analyze the clinical significance of MRVI1-AS1 in HCC. The functions of MRVI1-AS1 in HCC cells metastasis and growth were explored by transwell assays, wound healing assay, MTT assay, EdU assay, the intravenous transplantation tumor model, and the subcutaneous xenograft tumor model. Microarray mRNA expression analysis, dual luciferase assays, and actinomycin D treatment were used to explore the downstream target of MRVI1-AS1 in HCC cells. RIP assay was applied to assess the direct interactions between CELF2 and MRVI1-AS1 or SKA1 mRNA. Rescue experiments were employed to validate the functional effects of MRVI1-AS1, CELF2, and SKA1 on HCC cells. RESULTS: MRVI1-AS1 was found to be dramatically upregulated in HCC and the expression was strongly linked to tumor size, venous infiltration, TNM stage, as well as HCC patients' outcome. Cytological experiments and animal experiments showed that MRVI1-AS1 promoted HCC cells metastasis and growth. Furthermore, SKA1 was identified as the downstream targeted mRNA of MRVI1-AS1 in HCC cells, and MRVI1-AS1 increased SKA1 expression by recruiting CELF2 protein to stabilize SKA1 mRNA. In addition, we found that MRVI1-AS1 expression was stimulated by hypoxia through a HIF-1-dependent manner, which meant that MRVI1-AS was a direct downstream target gene of HIF-1 in HCC. CONCLUSION: In a word, our findings elucidated that hypoxia-induced MRVI1-AS1 promotes metastasis and growth of HCC cells via recruiting CELF2 protein to stabilize SKA1 mRNA, pointing to MRVI1-AS1 as a promising clinical application target for HCC therapy.

Erratum: Hypoxia-induced up-regulation of VASP promotes invasiveness and metastasis of hepatocellular carcinoma: Erratum.

[This corrects the article DOI: 10.7150/thno.26789.].

Isoliquiritigenin alleviates the development of alcoholic liver fibrosis by inhibiting ANXA2.

The study aimed to investigate the effect of isoliquiritigenin (ISL) on model of alcoholic liver fibrosis (ALF). C57BL/6 mice were used to establish animal model of ALF, HSC-T6 cells were used to establish alcohol-activated cell model, and tandem mass tag (TMT) assays were used to analyze the proteome. The results showed that ISL obviously alleviated hepatic fibrosis in model mice. ISL visually improved the area of liver pathological stasis and deposition of fibrillar collagen (Sirius Red staining, Masson staining), inhibited the mRNA expression levels of interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and interleukin 1ß (IL-1ß) in liver tissues. ISL down-regulated the mRNA expression levels of IL-6 and transforming growth factor-ß1(TGF-ß1) in activated hepatic stellate cells (HSCs). And ISL significantly reduced annexin A2 (ANXA2) in vitro detected by TMT proteomics technology. Interestingly, it was found for the first time that ISL could inhibit ANXA2 expression both in vivo and in vitro, block the sphingosine kinases (SPHKs)/sphingosine-1-phosphate (S1P)/interleukin 17 (IL-17) signaling pathway and regulate the expression of α-smooth muscle actin (α-SMA) by inhibiting the phosphorylation of signal transducer and activator of transcription 3 (STAT3) at the downstream signal to finally reverse HSCs activation and hepatic fibrosis. Thus, we demonstrated that ISL is a drug monomer with notable anti-hepatic fibrosis activity.

Effects of sling exercise on the core endurance and performance of basketball players / Efectos del ejercicio con sling en la resistencia del core y rendimiento de los jugadores de baloncesto / Efeitos do exercício com sling na resistência do core e desempenho de jogadores de basquetebol

ABSTRACT Introduction Strong core stability and strength enable the trunk to transfer the maximum amount of torque to the terminal segments, which is conducive to improving athletic performance. Because sling training is a new core exercise method, its effect on trunk endurance relative to basketball performance has rarely been studied. Objective To investigate whether a core exercise program in a specific sports group can improve core and sports-specific performance. Methods A total of 40 college students majoring in basketball were randomly assigned to training and control groups. A standardized set of core endurance and basketball-specific performance tests were used to determine and assess the effects of sling training on trunk strength, endurance, and control. Results Flexor, extensor, and right and left lateral trunk flexor muscles endurance were significantly greater in the training group than in the control group, and the time to complete the layup obstacle course was shorter than in the control group at the end of the training program, p<0.01. No differences between the two groups were found in the penalty shot, the fixed position shot, or the vertical jump and reach at the end of the training program. Conclusions Sling exercises can improve the core endurance and strength of basketball players and increase the speed of lay-ups over obstructions. Level of evidence I; Randomized clinical trial.

RESUMEN Introducción La sólida estabilidad y fuerza del core permiten que el tronco transfiera el torque máximo a los segmentos terminales, lo que conduce a mejorar el rendimiento deportivo. Como método novedoso de ejercicio para el core, se ha estudiado poco el efecto del entrenamiento con ejercicios con sling sobre la resistencia del tronco en relación con el rendimiento en el baloncesto. Objetivo Investigar si un programa de ejercicios para el core en un grupo deportivo específico puede mejorar el rendimiento del core y específico del deporte. Métodos Un total de 40 estudiantes universitarios con especialización en baloncesto fueron asignados aleatoriamente a grupos de entrenamiento y de control. Se utilizó una serie estandarizada de pruebas de resistencia del core y rendimiento específico del baloncesto para determinar y evaluar los efectos de los ejercicios con sling en la fuerza, la resistencia y el control del tronco. Resultados La resistencia de los músculos flexores, extensores y flexores laterales derecho e izquierdo del tronco fue significativamente mayor en el grupo de entrenamiento en comparación con el grupo de control, y el tiempo para completar la prueba de tiro con obstáculos fue menor que el del grupo de control al final del programa de entrenamiento, p<0,01. No hubo diferencias entre los dos grupos en lo que respecta a: tiro libre, lanzamiento en posición fija y salto vertical y alcance al final del programa de entrenamiento. Conclusiones Los ejercicios con sling pueden mejorar la resistencia y la fuerza del core en jugadores de baloncesto y aumentar la velocidad de los tiros con dribling. Nivel de evidencia I; Ensayo clínico aleatorizado.

RESUMO Introdução A sólida estabilidade e a força do core permitem que o tronco transfira o torque máximo para os segmentos terminais, o que é propício para melhorar o desempenho atlético. Como um novo método de exercício para o core, o efeito do treinamento com sling na resistência do tronco com relação ao desempenho no basquete tem sido pouco estudado. Objetivo Investigar se um programa de exercícios para o core em um grupo esportivo específico pode melhorar o desempenho do core e específico do esporte. Métodos Um total de 40 estudantes universitários formados em basquete foram aleatoriamente designados para grupos de treinamento e controle. Uma série padronizada de testes de resistência do core e desempenho específico do basquete foi usada para determinar e avaliar os efeitos dos exercícios com sling na força, resistência e controle do tronco. Resultados A resistência dos músculos flexores, extensores e flexores laterais direito e esquerdo do tronco foi significativamente maior no grupo treinamento em comparação ao grupo controle e o tempo para concluir o teste de bandeja com obstáculos foi menor que o do grupo controle no final do programa de treinamento, p < 0,01. Não houve diferenças entre os dois grupos quanto ao lance livre, arremesso em posição fixa e salto vertical e alcance no final do programa de treinamento. Conclusões Os exercícios com sling podem melhorar a resistência e a força do core em jogadores de basquete e aumentar a velocidade das bandejas com drible. Nível de evidência I; Estudo clínico randomizado.

The crosstalk between sonodynamic therapy and autophagy in cancer.

As a noninvasive treatment approach for cancer and other diseases, sonodynamic therapy (SDT) has attracted extensive attention due to the deep penetration of ultrasound, good focusing, and selective irradiation sites. However, intrinsic limitations of traditional sonosensitizers hinder the widespread application of SDT. With the development of nanotechnology, nanoparticles as sonosensitizers or as a vehicle to deliver sonosensitizers have been designed and used to target tissues or tumor cells with high specificity and accuracy. Autophagy is a common metabolic alteration in both normal cells and tumor cells. When autophagy happens, a double-membrane autophagosome with sequestrated intracellular components is delivered and fused with lysosomes for degradation. Recycling these cell materials can promote survival under a variety of stress conditions. Numerous studies have revealed that both apoptosis and autophagy occur after SDT. This review summarizes recent progress in autophagy activation by SDT through multiple mechanisms in tumor therapies, drug resistance, and lipid catabolism. A promising tumor therapy, which combines SDT with autophagy inhibition using a nanoparticle delivering system, is presented and investigated.