Two‐step deposition method has been widely exploited to fabricate FA1‐xCsxPbI3 perovskite solar cells. However, in previous studies, CsI is mainly added into the PbI2 precursor with DMF/DMSO as ...solvent. Here in this study, a novel method to fabricate FA1‐xCsxPbI3 perovskite has been proposed. The CsI is simultaneously added into the PbI2 precursor and the organic FAI/MACl salts solution in our modified two‐step deposition process. The resulting FA1‐xCsxPbI3 film exhibits larger perovskite crystals and suppressed defect density (4.05×1015 cm−3) compared with the reference perovskite film (9.23×1015 cm−3) without CsI. Therefore, the obtained FA1‐xCsxPbI3 perovskite solar cells have demonstrated superior power conversion efficiencies (PCE=21.96 %) together with better long‐term device stability.
CsI is simultaneously added into PbI2 precursor and organic FAI solution in the two‐step deposition method to promote the film quality of FA1‐xCsxPbI3 film. Therefore, our modified two‐step deposition method could contribute to perovskite solar cells with superior performance.
In 2012, we briefly summarized the mechanisms, pathophysiological roles and methods for analyzing mitophagy. As then, the mitophagy field has continued to grow rapidly, and many new molecular ...mechanisms regulating mitophagy and molecular tools for monitoring mitophagy have been discovered and developed. Therefore, the purpose of this review is to update information regarding these advances in mitophagy while focusing on basic molecular mechanisms of mitophagy in different organisms and its pathophysiological roles. We also discuss the advantage and limitations of current methods to monitor and quantify mitophagy in cultured cells and in vivo mouse tissues.
The past decade has witnessed the occurrence of novel 2D moiré patterns in nanoflatland materials. These visually beautiful moiré superlattices have become a playground on which exotic quantum ...phenomena can be observed. The state‐of‐the‐art experimental techniques that have been developed for crafting moiré superlattices of flatland materials are reviewed. Graphene and its heterostructure with boron nitride have now sparked new interlayer twists as a new degree of freedom for tuning several angle‐dependent physical properties, e.g., the appearance of van Hove singularities, tunable Mott insulator states, and the Hofstadter butterfly pattern. Moreover, the interplay of correlated insulating states and superconductivity is recently observed for a so‐called magic‐angle twisted bilayer graphene. Furthermore, beyond graphene, other 2D materials, such as silicene, phosphorene, and the recent black phosphorus /MoS2 heterojunctions, which are 2D allotropes of bismuth and antimony grown on highly ordered pyrolytic graphite and MoS2, are considered. Finally, the optically important exciton phenomenon, which depends on the moiré potential and has been observed for a moiré superlattice of transition metal dichalcogenides, is discussed. This overview aims to cover all the fascinating prospects that depend on the moiré superlattice, ranging from electronic structure to optical exotics among flatland materials.
Moiré patterns are produced under twisted flatland materials with a fascinating quantum phenomenon. State‐of‐the‐art experimental techniques developed for crafting moiré superlattices are reviewed. In particular, special attention is paid to several twist angle‐dependent electronic properties that include appearance of van Hove singularities, tunable Mott insulator states, the Hofstadter butterfly pattern, correlated insulating states, superconductivity and moiré excitones observed for moiré heterostructures.
Mitochondria are cellular energy powerhouses that play important roles in maintaining cell survival, cell death and cellular metabolic homeostasis. Timely removal of damaged mitochondria via ...autophagy (mitophagy) is thus critical for cellular homeostasis and function. Mitochondria are reticular organelles that have high plasticity for their dynamic structures and constantly undergo fission and fusion as well as movement through the cytoskeleton. In this review, we discuss the most recent progress on the molecular mechanisms and roles of mitochondrial fission/fusion and mitochondrial motility in mitophagy. We also discuss multiple pathways leading to the quality control of mitochondria in addition to the traditional mitophagy pathway under different conditions.
Alcoholic liver disease (ALD) is a major health problem in the United States and worldwide without successful treatments. Chronic alcohol consumption can lead to ALD, which is characterized by ...steatosis, inflammation, fibrosis, cirrhosis, and even liver cancer. Recent studies suggest that alcohol induces both cell death and adaptive cell survival pathways in the liver, and the balance of cell death and cell survival ultimately decides the pathogenesis of ALD. This review summarizes the recent progress on the role and mechanisms of apoptosis, necroptosis, and autophagy in the pathogenesis of ALD. Understanding the complex regulation of apoptosis, necrosis, and autophagy may help to develop novel therapeutic strategies by targeting all 3 pathways simultaneously.
Cell death and cell survival are closely associated with alcoholic liver disease.
Ethanol metabolism leads to increased oxidative stress resulting in mitochondrial damage and apoptosis in hepatocytes.
Chronic alcohol consumption increases gut permeability and elevated systemic levels of gut‐derived endotoxins resulting in increased production of TNF‐α from activated Kupffer cells.
Depending on the cIAP levels and caspase‐8 activation in hepatocytes, TNF‐α either induces apoptosis or necroptosis by activating Bid‐mediated mitochondrial apoptotic pathway or ripoptosome or necrosome.
Relativistic heavy-ion experiments have observed similar quenching effects for (prompt) D mesons compared to charged hadrons for transverse momenta larger than 6-8 GeV, which remains a mystery since ...heavy quarks typically lose less energies in quark-gluon plasma than light quarks and gluons. Recent measurements of the nuclear modification factors of B mesons and B-decayed D mesons by the CMS Collaboration provide a unique opportunity to study the flavor hierarchy of jet quenching. Using a linear Boltzmann transport model combined with hydrodynamics simulation, we study the energy loss and nuclear modification for heavy and light flavor jets in high-energy nuclear collisions. By consistently taking into account both quark and gluon contributions to light and heavy flavor hadron productions within a next-to-leading order perturbative QCD framework, we obtain, for the first time, a satisfactory description of the experimental data on the nuclear modification factors for charged hadrons, D mesons, B mesons and B-decayed D mesons simultaneously over a wide range of transverse momenta (8-300 GeV). This presents a solid solution to the flavor puzzle of jet quenching and constitutes a significant step towards the precision study of jet-medium interaction. Our study predicts that at transverse momenta larger than 30-40 GeV, B mesons also exhibit similar suppression effects to charged hadrons and D mesons, which may be tested by future measurements.
Liver is the major organ that regulates whole body cholesterol metabolism. Disrupted hepatic cholesterol homeostasis contributes to the pathogenesis of nonalcoholic steatohepatitis, dyslipidemia, ...atherosclerosis, and cardiovascular diseases. Hepatic bile acid synthesis is the major catabolic mechanism for cholesterol elimination from the body. Furthermore, bile acids are signaling molecules that regulate liver metabolism and inflammation. Autophagy is a highly-conserved lysosomal degradation mechanism, which plays an essential role in maintaining cellular integrity and energy homeostasis. In this review, we discuss emerging evidence linking hepatic cholesterol and bile acid metabolism to cellular autophagy activity in hepatocytes and macrophages, and how these interactions may be implicated in the pathogenesis and treatment of fatty liver disease and atherosclerosis.
•Disrupted cholesterol homeostasis is critically implicated in the pathogenesis of fatty liver disease and atherosclerosis.•Autophagy regulates organelle homeostasis and cellular integrity.•New studies show that cholesterol and bile acids modulate hepatic autophagy.•Autophagy regulates macrophage cholesterol homeostasis in atherosclerosis.
Autophagy in liver diseases: A review Qian, Hui; Chao, Xiaojuan; Williams, Jessica ...
Molecular aspects of medicine,
December 2021, 2021-Dec, 2021-12-00, 20211201, Letnik:
82
Journal Article
Recenzirano
Odprti dostop
The liver is a highly dynamic metabolic organ that plays critical roles in plasma protein synthesis, gluconeogenesis and glycogen storage, cholesterol metabolism and bile acid synthesis as well as ...drug/xenobiotic metabolism and detoxification. Research from the past decades indicate that autophagy, the cellular catabolic process mediated by lysosomes, plays an important role in maintaining cellular and metabolic homeostasis in the liver. Hepatic autophagy fluctuates with hormonal cues and the availability of nutrients that respond to fed and fasting states as well as circadian activities. Dysfunction of autophagy in liver parenchymal and non-parenchymal cells can lead to various liver diseases including non-alcoholic fatty liver diseases, alcohol associated liver disease, drug-induced liver injury, cholestasis, viral hepatitis and hepatocellular carcinoma. Therefore, targeting autophagy may be a potential strategy for treating these various liver diseases. In this review, we will discuss the current progress on the understanding of autophagy in liver physiology. We will also discuss several forms of selective autophagy in the liver and the molecular signaling pathways in regulating autophagy of different cell types and their implications in various liver diseases.
Autophagy is a lysosomal degradation pathway that degrades cytoplasmic proteins and organelles. Absence of autophagy in hepatocytes has been linked to promoting liver injury and tumorigenesis; ...however, the mechanisms behind why a lack of autophagy induces these complications are not fully understood. The role of mammalian target of rapamycin (mTOR) in impaired autophagy‐induced liver pathogenesis and tumorigenesis was investigated by using liver‐specific autophagy related 5 knockout (L‐ATG5 KO) mice, L‐ATG5/mTOR, and L‐ATG5/Raptor double knockout (DKO) mice. We found that deletion of mTOR or Raptor in L‐ATG5 KO mice at 2 months of age attenuated hepatomegaly, cell death, and inflammation but not fibrosis. Surprisingly, at 6 months of age, L‐ATG5/mTOR DKO and L‐ATG5/Raptor DKO mice also had increased hepatic inflammation, fibrosis, and liver injury, similar to the L‐ATG5 KO mice. Moreover, more than 50% of L‐ATG5/mTOR DKO and L‐ATG5/Raptor DKO mice already developed spontaneous tumors, but none of the L‐ATG5 KO mice had developed any tumors at 6 months of age. At 9 months of age, all L‐ATG5/mTOR DKO and L‐ATG5/Raptor DKO had developed liver tumors. Mechanistically, L‐ATG5/mTOR DKO and L‐ATG5/Raptor DKO mice had decreased levels of hepatic ubiquitinated proteins and persistent nuclear erythroid 2 p45‐related factor 2 activation but had increased Akt activation compared with L‐ATG5 KO mice. Conclusion: Loss of mTOR signaling attenuates the liver pathogenesis in mice with impaired hepatic autophagy but paradoxically promotes tumorigenesis in mice at a relatively young age. Therefore, the balance of mTOR is critical in regulating the liver pathogenesis and tumorigenesis in mice with impaired hepatic autophagy.
Acetaminophen (APAP) overdose is a major cause of hepatotoxicity and acute liver failure in the U.S., but the pathophysiology is incompletely understood. Despite evidence for apoptotic signaling, ...hepatic cell death after APAP is generally considered necrotic in mice and in humans. Recent findings suggest that the receptor interacting protein kinase 3 (RIP3) acts as a switch from apoptosis to necrosis (programmed necrosis). Thus, the aim of the current investigation was to determine if RIP3 is involved in APAP‐induced liver cell death. APAP (200‐300 mg/kg) caused glutathione depletion and protein adduct formation, oxidant stress, mitochondrial release of apoptosis inducing factor, and nuclear DNA fragmentation resulting in centrilobular necrosis in C57Bl/6J mice. Inhibiting RIP3 protein induction with antisense morpholinos in wild‐type animals or using RIP3‐deficient mice had no effect on protein adduct formation but attenuated all other parameters, including necrotic cell death, at 6 hours after APAP. In addition, cultured hepatocytes from RIP3‐deficient mice showed reduced injury compared to wild‐type cells after 24 hours. Interestingly, APAP‐induced mitochondrial translocation of dynamin‐related protein 1 (Drp1), the initiator of mitochondrial fission, was inhibited by reduced RIP3 protein expression and the Drp1 inhibitor MDIVI reduced APAP‐induced cell death at 24 hours. All of these protective effects were lost after 24 hours in vivo or 48 hours in vitro. Conclusion: RIP3 is an early mediator of APAP hepatotoxicity, involving modulation of mitochondrial dysfunction and oxidant stress. Controlling RIP3 expression could be a promising new approach to reduce APAP‐induced liver injury, but requires complementary strategies to control mitochondrial dysfunction for long‐term protection. (Hepatology 2013; 58:2099–2108)
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