Hydrodeoxygenation (HDO) is a key process for upgrading lignin derived bio-oil to high-quality fuels and chemicals. In this study, CoxNiyAl-T catalysts with varying Co/Ni molar ratios and calcination temperatures were fabricated through flash Joule heating assisted carbon coating, with layered double hydroxides (LDHs) adopted as precursors. These catalysts were used for the hydrodeoxygenation of vanillin to 4-methylcyclohexanol (MCH). Under the optimized reaction conditions (180 °C, 2.5 h, 1 MPa N2) with isopropanol serving as both hydrogen donor and solvent, the Co1Ni2Al-850 catalyst achieved nearly 100% vanillin conversion and a 94.3% yield of MCH. Based on various characterization results, Co1Ni2Al-850 catalysts exhibited suitable specific surface area, pore structure and acid sites. The excellent performance of Co1Ni2Al-850 catalyst was also attributed to the Co-Ni synergistic effect: Ni species accelerated the activation and dissociation of isopropanol to supply sufficient active hydrogen species for HDO; Co species promoted removal of methoxy groups in MMP. In addition, the presence of Al enhanced the structural stability. Based on the product distribution and characterization results, the possible reaction mechanism of the catalytic system was proposed. This study provides a new way for the development of efficient non noble metal catalysts for the hydrodeoxygenation system of biomass derivatives.

Catalytic hydrodeoxygenation (HDO) is a pivotal strategy for upgrading lignin-derived oxygen-rich compounds into value-added chemicals. Developing high-performance non-precious metal inorganic catalysts with precisely controllable active sites remains a core challenge in this field. Herein, we reported a facile one-pot hydrothermal-calcination reduction method to construct carbon-confined Co-CoOx dual-site catalysts (Cox@Say-T) using salicylic acid as a bifunctional organic ligand and in-situ carbon source. The optimized Co5@Sa5–550 catalyst exhibited outstanding performance in the transfer HDO of guaiacol to cyclohexanol, achieving 99.3% guaiacol conversion and 93.5% cyclohexanol selectivity under mild conditions (180 °C, 2 MPa N2, 4 h) with isopropanol as the hydrogen donor, eliminating the need for external H2. Comprehensive structural characterizations demonstrated that the superior catalytic activity originates from the synergistic effect of uniformly dispersed Co-CoOx sites. Metallic Co centers catalyzed isopropanol dehydrogenation to generate active hydrogen species, while CoOx species acted as moderate Lewis acid sites to facilitate methoxy group adsorption and CO bond cleavage. This work provided a controllable and scalable strategy for designing efficient non-precious metal inorganic catalysts for biomass valorization.

Rationale: Liver regeneration is regulated by both metabolic processes and immune responses. Nonetheless, there is limited comprehension of the mechanisms involved. PINK1/Parkin-mediated mitophagy has been well documented, the role and underlying alternative mechanism of PINK1/Parkin in regulating mitochondrial metabolism during liver regeneration remains unclear. Methods: Liver tissues from mice undergoing hepatectomy were utilized to evaluate the expression levels of PINK1/Parkin. Hepatocyte-specific PINK1 knockout and transgenic mouse models were generated to investigate the impact of PINK1 on regeneration. Mass spectrometry, co-immunoprecipitation, and ubiquitination assays were performed to explore the underlying molecular mechanisms. Results: We observed PINK1/Parkin expression was markedly upregulated in hepatic tissue following liver resection. PINK1 depletion in hepatocytes caused impaired liver regeneration. Moreover, mitochondrial calcium overload was found be responsible for restricted TCA by inhibiting succinate dehydrogenase activity in PINK1 deficient hepatocytes. Interestingly, PINK1 deficiency leads to succinate accumulation and release from hepatocytes, which impairs liver regeneration by restricting macrophage pro-repair phenotypes. This effect was further confirmed by enhanced regeneration in myeloid SUCNR1 knockout mice. Mechanistically, Sigma-1 is a molecular chaperone of the endoplasmic reticulum calcium channel IP3R, which helps maintain its normal functional conformation. Parkin was able to bind Sigma-1 through its UBL domain, facilitating its k48-linked ubiquitination, which promotes Sigma-1 degradation and subsequently suppressing calcium transfer from the ER to mitochondria at the mitochondrial-associated ER membrane. Conclusions: Collectively, PINK1/Parkin signaling regulates hepatocellular mitochondrial ATP and succinate production by modulating ER-mitochondria calcium transfer to promote liver regeneration, revealing a promising therapeutic target for liver regeneration.

The brushless doubly-fed induction generators (BDFIGs) with complex internal magnetic coupling, suffer from parameter perturbations in the control systems when the temperature and frequency of the system change. This paper proposes a non-cascaded fractional order sliding mode (FOSM) control strategy for the BDFIG to compensate the mismatched uncertainties structured by parameter perturbations. For both balanced and unbalanced load systems, the mismatched uncertainties in the mathematical models of BDFIGs are thoroughly analyzed and modeled. For this second-order nonlinear system subject to mismatched uncertainties, a fractional-order sliding surface and a chattering-free control law are designed within the non-cascaded controller. This approach significantly enhances the accuracy, dynamic response, and robustness against uncertainties in the BDFIG control system, thereby reducing voltage fluctuations in standalone power generation systems and optimizing the three-phase balance of the output voltage. Finally, experimental results demonstrate that the proposed control strategy effectively improves system performance and exhibits significant superiority.

BACKGROUND:Precise regulation of mitochondrial function is critical for liver regeneration. However, the underlying regulatory mechanism remains elusive. Here, we aimed to investigate the role of hepatocellular glutathione peroxidase 3 (GPX3) in liver regeneration. METHODS:In a 70% partial hepatectomy (PH) mouse model, immunostaining and single-cell RNA sequencing revealed significant enrichment but down-regulation of mitochondrial oxidative phosphorylation pathways post-PH, along with up-regulated hypoxia-inducible factor 1a (HIF-1a) and GPX3 in hepatocytes. Single-cell analysis confirmed peak GPX3 expression in hepatocytes at day 2 post-PH. Hepatocyte-specific GPX3 knockout impaired mitochondrial function and delayed liver regeneration. RESULTS:Mechanistically, immunoprecipitation-mass spectrometry and MitoCarta3.0 analysis identified voltage-dependent anion channel 1 (VDAC1) as a direct GPX3-binding partner. GPX3 interacted with VDAC1 via its A2 domain (residues 75-150), suppressing VDAC1 oligomerisation to restore mitochondrial Ca2+ homeostasis and preserve mitochondrial quality control (MQC). Notably, GPX3 deficiency promoted mitochondrial DNA (mtDNA) release, activating the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway in macrophages. Persistent STING hyperactivation increased interferon production while suppressing hepatocyte growth factor release, further inhibiting regeneration. Critically, GPX3 overexpression enhanced liver regeneration in both PH and hepatic ischemia-reperfusion injury models, underscoring its central role across regenerative stressors. CONCLUSIONS:In conclusion, GPX3 promotes liver regeneration by inhibiting VDAC1 oligomerisation to stabilise mitochondrial Ca2+ dynamics and MQC, while preventing mtDNA-mediated functional and phenotypic alterations in macrophages, positioning it as a therapeutic target for liver regeneration. KEY POINTS:GPX3 directly binds VDAC1 via its A2 domain to suppress VDAC1 oligomerisation, restoring mitochondrial Ca2 + homeostasis and preserving mitochondrial quality control during liver regeneration. GPX3 deficiency promotes mtDNA release, hyperactivating the cGAS-STING pathway in macrophages and suppressing hepatocyte growth factor (HGF) release. GPX3 overexpression enhances liver regeneration in both partial hepatectomy and hepatic ischemia-reperfusion injury models, highlighting its therapeutic potential.

This study proposes an improved super-twisting sliding mode (STSM) control method for a brushless doubly fed induction generator (BDFIG) used in standalone ship shaft power generation systems. Focusing on the problem of the low tracking accuracy of the power winding (PW) voltages caused by the parameter perturbation of BDFIG systems, a mismatched uncertain model of the BDFIG is constructed. Additionally, an improved STSM control method is proposed to address the power load variation and compensate for the mismatched uncertainty through virtual control technology. Based on the direct vector control of the control winding (CW), the proposed method ensured that the voltage amplitude error of the power winding could converge to the equilibrium point rather than the neighborhood. Finally, in the experimental investigation of the BDFIG-based ship shaft independent power system, the dynamic performance in the startup and power load changing conditions were analyzed. The experimental results show that the proposed improved STSM controller has a faster dynamic response and higher steady-state accuracy than the proportional integral control and the linear sliding mode control, with strong robustness to the mismatched uncertainties caused by parameter perturbations.

Catalytic upgrading of lignin-derived bio-oil to value-added chemicals was of great significance for the utilization of biomass resources. Hydrodeoxygenation (HDO) was widely regarded as a promising pathway for the upgrading of lignin-derived bio-oil. And the key to this issue was to develop effective and sustainable catalysts. In this study, a series of lignin-derived carbon-based highly effective catalysts were synthesized through a one-step hydrothermal method for the catalytic HDO of lignin and its derivatives. Then, lignin-MOF-derived catalysts (nCo-TPA/C-T) were successfully applied to the catalytic HDO of lignin-derived phenolics. All catalysts were characterized in detail to investigate the relationships between physicochemical properties and their catalytic performances. The results demonstrated that the catalyst 2Co-TPA/C-500 exhibited excellent catalytic activity in the conversion of vanillin (VAN) to 2-methoxy-4-methylphenol (MMP) in mild condition (160 degrees C, 0.5 MPa N2, and 1 h), without the presence of external hydrogen. The conversion of VAN was up to nearly 100 %, with a high selectivity of MMP (about 94.5 %). It was confirmed that the excellent catalytic performance was related to types of organic ligands, metal-ligand ratio, catalyst calcination temperature, etc. The catalysts also exhibited good activity for other lignin-derived phenols. This work could offer a useful strategy for the catalytic upgrading of lignin-derived phenolics into value-added chemicals.

Background & Aims: Efferocytosis is essential for maintaining tissue homeostasis and resolving inflammation, but this process is compromised during sepsis. This study aimed to elucidate the role of neurite outgrowth inhibitor protein B (Nogo-B) in regulating macrophage efferocytosis under septic conditions and to evaluate its potential as a therapeutic target. Methods: We evaluated Nogo-B expression and efferocytosis in monocytes and monocyte-derived macrophages (MDMs) under septic conditions. Myeloid-specific Nogo deletion was used to assess its impact on MDM efferocytosis and septic organ injury. Mechanistic studies examined HIF-1α/ADAM17 signaling, mitochondrial calcium dynamics, metabolic activity, and endoplasmic reticulum (ER) stress. INCB081776, a dual MerTK/AXL inhibitor, was administered in vivo to suppress efferocytosis before mouse modeling. Statistical comparisons were performed using t tests or ANOVA. Results: Septic conditions upregulated Nogo-B expression and impaired efferocytosis in monocytes and MDMs, but not in peritoneal macrophages or Kupffer cells (n = 3–7, p <0.05). Myeloid Nogo deficiency significantly enhanced MDM efferocytosis and alleviated inflammatory liver and lung injury (n = 7, p <0.05). Mechanistically, Nogo-B disrupted ER–mitochondria calcium transfer, reduced mitochondrial calcium levels, and suppressed isocitrate dehydrogenase and succinate dehydrogenase activities. This led to impaired tricarboxylic acid (TCA) cycle function and oxidative phosphorylation (OXPHOS), resulting in succinate accumulation and an elevated succinate/α-ketoglutarate ratio. The metabolic shift activated HIF-1α/ADAM17 signaling, promoting MerTK/AXL cleavage and further impairing efferocytosis. Nogo deficiency also promoted MDM M2 polarization without affecting ER stress under lipopolysaccharide stimulation. Pharmacological inhibition of MerTK/AXL reversed the beneficial effects of myeloid Nogo deficiency on efferocytosis and septic liver and lung injury (n = 5, p <0.05). Conclusions: Nogo-B impairs MDM efferocytosis by suppressing OXPHOS and activating HIF-1α/ADAM17 signaling, thereby exacerbating septic liver and lung injury. Targeting Nogo-B offers a novel strategy to restore efferocytosis and alleviate sepsis. Impact and implications: Efferocytosis is compromised during sepsis, contributing to enhanced inflammation and organ damage. Our study identified Nogo-B as a critical mediator linking disrupted mitochondrial calcium uptake to impaired MDM efferocytosis. Targeting Nogo-B may represent a novel therapeutic strategy to restore efferocytosis and attenuate sepsis-related tissue injury. Further translational studies are needed to validate these findings in human disease.

BACKGROUND:This study investigates the role and mechanism of neutrophil extracellular trap (NET) clearance by aged macrophages during sepsis-induced liver injury, as elderly patients show higher rates of organ damage and mortality in sepsis. METHODS:A sepsis model was established using cecal ligation and puncture (CLP) in aged (100-week-old) and young mice (8-week-old) to study NET clearance by macrophages, assessing liver injury and inflammatory responses with interventions targeting AMP-dependent protein kinase (AMPK) and phagocytosis pathways. Additionally, the study included 40 sepsis patients, with 25 elderly (65-89 years) and 15 young (31-62 years) individuals, and collected peripheral blood samples from all for in vitro experiments. RESULTS:In aged mice, a significant increase in 7-day mortality was observed (hazard ratio [HR] = 2.50, 95% confidence interval [CI], 1.10-5.65, P = .009), alongside heightened inflammatory response and liver injury (histopathology score: 3.2 ± 0.4 vs 2.4 ± 0.6; P = .021), compared to young mice post-CLP. Hepatic NET accumulation markedly increased (mean difference [MD] = 0.43%, 95% CI, 0.25%-0.61%; P < .001), which was attenuated by DNase I-mediated NET inhibition, reducing hepatic enzymes and inflammatory responses. Consistently, transplantation of young bone marrow into aged recipients significantly reduced NET accumulation (MD = -0.33%, 95% CI, -0.43% to -0.22%; P < .001). Mechanistically, the phosphorylation of AMPK (0.68-fold vs young; P < .001) and Ca 2+ /calmodulin-dependent protein kinase kinase 2 (CaMKK2) was suppressed in aged septic mice. Activation of AMPK via 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) led to a decrease in hepatic NET accumulation (MD = -0.30%, 95% CI, -0.41% to -0.19%; P < .001), improved liver injury (histopathology score: 2.49 ± 0.24 vs 3.07 ± 0.28; P = .006), and reduced 7-day mortality (HR = 0.37, 95% CI, 0.15-0.94, P = .038). Critically, elderly patients exhibited elevated NET-related markers, compounded by suppressed AMPK phosphorylation and impaired NET phagocytosis (MD = -16.34%, 95% CI, -24.31% to -8.37%; P = .002). CONCLUSIONS:Aging impairs AMPK-mediated macrophage clearance of NETs in the liver, exacerbating liver inflammatory injury. Focusing on NETs could offer a therapeutic strategy to mitigate liver damage and reduce mortality in elderly sepsis patients.

This article proposes a new adaptive gain, full-order terminal sliding mode control algorithm for the speed regulation of a surface-mounted permanent magnet synchronous motor (SPMSM) control system. To deal with the mismatched uncertainties in the double-loop nonlinear system of the SPMSMs, a virtual control technique is constructed with the full-order terminal sliding mode control to ensure that the tracking error trajectory can converge to equilibrium in finite time. Owing to the integral control law, the output signals of the controllers are smoothed, with the chattering phenomenon attenuated and the gain-margin overestimation avoided. Comprehensive simulation and experimental results have been carried out to demonstrate the superiority of the proposed method in improving tracking accuracy, rapidness, and robustness to the matched and mismatched uncertainties.

Lignin represents a significant source of aromatic hydrocarbons in the natural world. The production of high- value chemicals from lignin has the great potential to effectively address the issue of fossil energy scarcity. In this study, complex sulfides of nickel-cobalt bimetallic catalysts were prepared via hydrothermal synthesis and subsequently employed in the catalytic hydrogenolysis of C-O bonds present in lignin. A series of complex sulfides Ni3S2/Co3S4-CSn-x-T derived from lignin-MOF (n = 0.5, 1, 1.5 and 2; x = 2, 4 and 6; T = 400, 500, 600 and 700 degrees C), were prepared under different conditions and subsequently employed in the catalytic hydrogenolysis of lignin model compounds. The optimal catalyst Ni3S2/Co3S4-CS1-4-500 exhibited the highest conversion rate of benzyl phenyl ether (BPE) (about 97.3 %), and the yields of toluene and phenol produced were 49.5 % and 43.6 %, respectively with isopropanol as the reaction solvent and no external H2. The introduction of element sulfur in catalysts could effectively inhibit the further hydrogenation of generated aromatic chemicals. The catalysts were well characterized, and the results demonstrated that the catalysts exhibited high catalytic activity with an increased loading of active components. This study provided some novel findings for the construction of biomass-based catalysts and the production lignin-derived aromatic chemicals.

Background & Aims: Autophagy plays an important role in liver regeneration. However, most studies are limited to hepatocytes, and the function and mechanism of macrophage autophagy in liver regeneration remain unclear. This study investigated the role of the essential autophagy gene encoding autophagy-related 16-like 1 (ATG16L1), which regulates the macrophage phenotype in liver regeneration. Methods: We generated FloxP-Atg16l1 (Atg16l1FL/FL), Lyz2-Cre Atg16l1 knockout (KO) (Atg16l1M-KO), and myeloid-specific Atg16l1-overexpression-knock-in (Atg16l1OE) mice. These mice were subjected to 70% partial hepatectomy to demonstrate the role of ATG16L1 in macrophages during liver regeneration. Results: ATG16L1 expression was significantly upregulated in macrophages during the early stages of liver regeneration. ATG16L1 deletion in macrophages substantially delayed liver regeneration in mice and caused a marked imbalance in Ly6Chi and Ly6Clo macrophage proportions in the liver. RNA-sequencing analysis revealed that, compared with macrophages isolated from Atg16l1FL/FL mice, those from Atg16l1M-KO mice exhibited significant downregulation of genes associated with oxidative phosphorylation and upregulation of proinflammatory gene expression. Mechanistically, ATG16L1 loss impaired mitophagy in macrophages, leading to the accumulation of mitochondrial damage and a metabolic shift that promoted proinflammatory macrophage polarization. ATG16L1 deficiency not only promoted macrophage mitochondrial (mt)DNA release and cyclic GMPAMP synthase-stimulator of interferon genes (STING) activation, but also suppressed STING degradation. Sustained STING hyperactivation and subsequent increased release of downstream interferons further contributed to the inhibition of liver regeneration. Notably, pharmacological activation or genetic overexpression of ATG16L1 significantly enhanced liver regeneration in mice. Conclusions: ATG16L1 has a pivotal role in liver regeneration by affecting the phenotype and function of macrophages. Thus, targeting ATG16L1 in macrophages could present a novel strategy for promoting liver regeneration. (c) 2025 The Authors. Published by Elsevier B.V. on behalf of European Association for the Study of the Liver (EASL). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

BACKGROUND & AIMS:Acute drug-induced liver injury (DILI) is a major cause of acute liver dysfunction and even liver failure. Peritoneal macrophages have been reported to invade into the injured liver for tissue repair. Herein, we aimed to investigate the role of autophagy-related 16 like 1 gene (ATG16L1) in regulating the reparative function of peritoneal macrophages during DILI caused by acetaminophen (APAP). METHODS:Myeloid ATG16L1 knockout (KO), overexpression (KI) or wild-type (WT) mice were challenged with a single dose of intraperitoneal APAP (300 mg/kg) injection. Intraperitoneal injection or depletion of peritoneal macrophages was conducted for the in vivo analysis. Co-culture of primary hepatocytes and peritoneal macrophages were applied for in vitro analysis. RESULTS:Peritoneal macrophages were able to rapidly invade into the liver in response to DILI. Peritoneal macrophage injection promoted, and peritoneal macrophage depletion impaired the resolution of inflammation and liver repair post DILI. DILI triggered ATG16L1 expression in intrahepatic accumulated peritoneal macrophages. Interestingly, compared with WT or KI peritoneal macrophages, KO peritoneal macrophages showed enhanced intrahepatic migration ability via Schlafen family member 5 (SLFN5)-CD44 signaling pathway, leading to less injury at early time of 24 hours post DILI in mice with KO peritoneal macrophage infusion. In addition, ATG16L1-mediated autophagy promoted phagocytosis and reparative phenotype of peritoneal macrophages by regulating reactive oxygen species (ROS)-Mer tyrosine kinase (MerTK) signaling. Moreover, peritoneal macrophage ATG16L1 promoted hepatocyte proliferation dependent on the interleukin (IL)-10-C-X-C motif chemokine receptor 2 (CXCR2) axis. CONCLUSIONS:ATG16L1 activation enhanced peritoneal macrophage phagocytosis and reparative phenotype via autophagy-ROS-MerTK signaling and promoted IL-10-CXCR2-dependent hepatocyte proliferation during DILI. Peritoneal macrophage ATG16L1 might be a novel therapeutic target for DILI.

The conversion of abundant lignin was of great significance for the utilization of biomass resources. In this study, lignin sulfonate (LS) was selected as a carbon-based support, which was successfully introduced into the NiCoMOF structure. A series of lignin and MOF hybrid catalysts (NinCo-MOF-LS) with varying metal ratios of Ni and Co were synthesized via the hydrothermal method. Subsequently, the catalytic hydrogenolysis of lignin-derived dimers was conducted over a range of NinCo-MOF-LS, with the impact of calcination temperature and lignin addition in the catalysts taken into account. The selective conversion of benzyl phenyl ether (BPE) and other lignin dimers was achieved over the NinCo-MOF-LS catalyst with isopropanol serving as the hydrogen donor solvent in a nitrogen atmosphere. The Ni/Co metal ratio and calcination temperature were found to have a significant impact on the catalytic performance. Through a comprehensive investigation of various reaction parameters, including temperature, pressure, reaction time, and reaction solvent, it was determined that the catalyst exhibited excellent catalytic activity in the selective hydrogenolysis of BPE to cycloalkane and cyclohexanol. The optimal reaction conditions (240 degrees C, 4 h, 3 MPa N2) were found to be conducive to the effective conversion of BPE into methylcyclohexane and cyclohexanol. The combination of lignin and metal-organic framework represented a novel approach to the utilization of lignin resources and the upgrading of biomassderived chemicals.

To improve the disturbance rejection and rapid response of permanent magnet synchronous motors (PMSMs), traditional sliding mode control (SMC) has been commonly used. However, the SMC has a serious problem of chattering. To address this, this study introduces a chattering-free sliding mode speed controller (CFSMC). This controller is designed to enhance system robustness against internal parameter variations and mitigate chattering from high-frequency switching. Furthermore, in the current loop, the Model Predictive Current Control (MPCC) strategy is also adopted to further enhance the system's rapid response performance. The effectiveness and practicality of the proposed approach are validated through comprehensive simulations and experiments.

The traditional centralized control algorithm of distributed drive electric vehicle has complex matrix operation, poor real-time torque distribution, and fails to make full use of the structural advantages and fault-tolerant control ability of multi-motor drive. A multi-agent-based drive anti-skid full-order sliding mode control strategy is proposed to solve the problem of four-wheel cooperative control. Taking slip rate as the control target, a four-wheel cooperative control system based on multi-agent is established, and a full-order sliding mode fault-tolerant control strategy is proposed to realize the rapid synchronous control of the slip rates of the four wheels, thereby improving the stability and safety of distributed drive vehicles. The experimental results on the hardware-in-loop platform show that the designed sliding mode controller has faster convergence speed and reduced control signal chattering, resulting in better control performance. Real vehicle tests verify the feasibility of the fault-tolerant control algorithm on hardware equipment and its effectiveness while driving.

Full order terminal sliding mode (FOTSM) control is designed for two-port soft open point (SOP) in this paper. The structure of the two-port SOP includes rectifier side and inverter side. The control system on the rectifier side is proposed to stabilize the DC side voltage. A fast full-order terminal sliding mode controller is applied to the current loop to achieve accurate and rapid current tracking performance in the situation of parameter perturbation. And the chattering can be eliminated completely under the designed integral-type control law, so that the continue control signals can be obtained. The control system on the inverter side is proposed to regulate the output power. And the application the FOTSM controller realizes the flexible and accurate power adjustment under a disturbed condition. The SOP provides flexible and accurate power regulation in distribution network. The excellent dynamic performance and anti-disturbance ability of the designed controllers are demonstrated by the simulation results.

The efficient hydrogenolysis of C-O ether bonds in lignin is the key for producing bio-oil and high-value chemicals. In this work, we synthesized a series of Ni-MOF-derived porous carbon spheres anchored Ni catalysts (Ni/C-x-T) with different metal/ligand molar ratios and calcination temperatures through solvothermal and carbothermal reduction method, and evaluated their catalytic transfer hydrogenolysis (CTH) performance for lignin model compounds using isopropanol as H-donor. The Ni/C-2-400 catalyst exhibited the excellent CTH performance, affording almost 100 % conversion of 2-phenoxy-1-phenylethanol even at a low reaction temperature of 120 degrees C. It was worth noting that the further hydrogenation of hydrogenolysis products phenol and ethylbenzene could be controlled by adjusting the reaction conditions, achieving phenol and ethylbenzene as main products at 120 degrees C, cyclohexanol and ethylbenzene at 140 degrees C, and cyclohexanol and ethylcyclohexane at 200 degrees C for 4 h. Based on the characterization results, the high catalytic activity of Ni/C-2-400 was attributed to the good dispersion and small particle size of metal Ni particles. Mechanistic studies showed that the cleavage of C-O ether bonds was the main reaction pathway, and high temperature helped accelerate hydrogenolysis and subsequent hydrogenation. Moreover, the Ni/C-2-400 catalyst had good stability and applicability to other model compounds. This work could provide some help for the upgrading of lignin and its derivative.