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Biomedicine & Pharmacotherapy =... Oct 2023Iron, as an essential trace element for the organism, is vital for maintaining the organism's health. Excessive iron can promote reactive oxygen species (ROS)... (Review)
Review
Iron, as an essential trace element for the organism, is vital for maintaining the organism's health. Excessive iron can promote reactive oxygen species (ROS) accumulation, thus damaging cells and tissues. Ferroptosis is a novel form of programmed cell death distinguished by iron overload and lipid peroxidation, which is unique from autophagy, apoptosis and necrosis, more and more studies are focusing on ferroptosis. Recent evidence suggests that ferroptosis is associated with the development of female reproductive disorders (FRDs), including polycystic ovary syndrome (PCOS), premature ovarian insufficiency (POI), endometriosis (EMs), ovarian cancer (OC), preeclampsia (PE) and spontaneous abortion (SA). Pathways and genes associated with ferroptosis may participate in processes that regulate granulosa cell proliferation and secretion, oocyte development, ovarian reserve function, early embryonic development and placental oxidative stress. However, its exact mechanism has not been fully revealed. Therefore, our review systematically elaborates the occurrence mechanism of ferroptosis and its research progress in the development of FRDs, with a view to providing literature references for clinical targeting of ferroptosis -related pathways and regulatory factors for the management of FRDs.
Topics: Pregnancy; Humans; Female; Ferroptosis; Placenta; Apoptosis; Abortion, Spontaneous; Iron; Iron Overload
PubMed: 37660655
DOI: 10.1016/j.biopha.2023.115415 -
Biochimica Et Biophysica Acta. Reviews... Sep 2023Cell death is a fundamental physiological process that occurs in all organisms and is crucial to each organism's evolution, ability to maintain a stable internal... (Review)
Review
Cell death is a fundamental physiological process that occurs in all organisms and is crucial to each organism's evolution, ability to maintain a stable internal environment, and the development of multiple organ systems. Disulfidptosis is a new mode of cell death that is triggered when cells with high expression of solute carrier family 7 member 11 (SLC7A11) are exposed to glucose starvation to initiate the process of cell death. The disulfidptosis mechanism is a programmed cell death mode that triggers cell death through reduction-oxidation (REDOX) reactions and disulfur bond formation. In disulfidptosis, disulfur bonds play a crucial role and cause the protein in the cell to undergo conformational changes, eventually leading to cell death. This mode of cell death has unique characteristics and regulatory mechanisms in comparison with other modes of cell death. In recent years, an increasing number of studies have shown that the disulfidptosis mechanism plays a key role in the occurrence and development of a variety of diseases. For example, cancer, cardiovascular diseases, neurodegenerative diseases, and liver diseases are all closely related to cell disulfidptosis mechanisms. Therefore, it is of paramount clinical significance to conduct in-depth research regarding this mechanism. This review summarizes the research progress on the disulfidptosis mechanism, including its discovery history, regulatory mechanism, related proteins, and signaling pathways. Potential applications of the disulfidptosis mechanism in disease therapy and future research directions are also discussed. This mechanism represents another subversive discovery after ferroptosis, and provides both a fresh perspective and an innovative strategy for the treatment of cancer, as well as inspiration for the treatment of other diseases.
Topics: Humans; Cell Death; Apoptosis; Cardiovascular Diseases; Clinical Relevance; Biology
PubMed: 37451411
DOI: 10.1016/j.bbcan.2023.188955 -
Nature Reviews. Gastroenterology &... Sep 2023The metabolic, digestive and homeostatic roles of the liver are dependent on proper crosstalk and organization of hepatic cell lineages. These hepatic cell lineages are... (Review)
Review
The metabolic, digestive and homeostatic roles of the liver are dependent on proper crosstalk and organization of hepatic cell lineages. These hepatic cell lineages are derived from their respective progenitors early in organogenesis in a spatiotemporally controlled manner, contributing to the liver's specialized and diverse microarchitecture. Advances in genomics, lineage tracing and microscopy have led to seminal discoveries in the past decade that have elucidated liver cell lineage hierarchies. In particular, single-cell genomics has enabled researchers to explore diversity within the liver, especially early in development when the application of bulk genomics was previously constrained due to the organ's small scale, resulting in low cell numbers. These discoveries have substantially advanced our understanding of cell differentiation trajectories, cell fate decisions, cell lineage plasticity and the signalling microenvironment underlying the formation of the liver. In addition, they have provided insights into the pathogenesis of liver disease and cancer, in which developmental processes participate in disease emergence and regeneration. Future work will focus on the translation of this knowledge to optimize in vitro models of liver development and fine-tune regenerative medicine strategies to treat liver disease. In this Review, we discuss the emergence of hepatic parenchymal and non-parenchymal cells, advances that have been made in in vitro modelling of liver development and draw parallels between developmental and pathological processes.
Topics: Humans; Liver; Liver Diseases; Hepatocytes; Cell Differentiation; Cell Lineage
PubMed: 37208503
DOI: 10.1038/s41575-023-00775-2 -
Nature Reviews. Molecular Cell Biology Jan 2024The forkhead box protein O (FOXO, consisting of FOXO1, FOXO3, FOXO4 and FOXO6) transcription factors are the mammalian orthologues of Caenorhabditis elegans DAF-16,... (Review)
Review
The forkhead box protein O (FOXO, consisting of FOXO1, FOXO3, FOXO4 and FOXO6) transcription factors are the mammalian orthologues of Caenorhabditis elegans DAF-16, which gained notoriety for its capability to double lifespan in the absence of daf-2 (the gene encoding the worm insulin receptor homologue). Since then, research has provided many mechanistic details on FOXO regulation and FOXO activity. Furthermore, conditional knockout experiments have provided a wealth of data as to how FOXOs control development and homeostasis at the organ and organism levels. The lifespan-extending capabilities of DAF-16/FOXO are highly correlated with their ability to induce stress response pathways. Exogenous and endogenous stress, such as cellular redox stress, are considered the main drivers of the functional decline that characterizes ageing. Functional decline often manifests as disease, and decrease in FOXO activity indeed negatively impacts on major age-related diseases such as cancer and diabetes. In this context, the main function of FOXOs is considered to preserve cellular and organismal homeostasis, through regulation of stress response pathways. Paradoxically, the same FOXO-mediated responses can also aid the survival of dysfunctional cells once these eventually emerge. This general property to control stress responses may underlie the complex and less-evident roles of FOXOs in human lifespan as opposed to model organisms such as C. elegans.
Topics: Animals; Humans; Caenorhabditis elegans; Signal Transduction; Forkhead Transcription Factors; Aging; Longevity; Mammals
PubMed: 37710009
DOI: 10.1038/s41580-023-00649-0 -
Journal of Materials Chemistry. B Nov 2023Bioprinting, as a groundbreaking technology, enables the fabrication of biomimetic tissues and organs with highly complex structures, multiple cell types, mechanical... (Review)
Review
Bioprinting, as a groundbreaking technology, enables the fabrication of biomimetic tissues and organs with highly complex structures, multiple cell types, mechanical heterogeneity, and diverse functional gradients. With the growing demand for organ transplantation and the limited number of organ donors, bioprinting holds great promise for addressing the organ shortage by manufacturing completely functional organs. While the bioprinting of complete organs remains a distant goal, there has been considerable progress in the development of bioprinted transplantable tissues and organs for regenerative medicine. This review article recapitulates the current achievements of organ 3D bioprinting, primarily encompassing five important organs in the human body (, the heart, kidneys, liver, pancreas, and lungs). Challenges from cellular techniques, biomanufacturing technologies, and organ maturation techniques are also deliberated for the broad application of organ bioprinting. In addition, the integration of bioprinting with other cutting-edge technologies including machine learning, organoids, and microfluidics is envisioned, which strives to offer the reader the prospect of bioprinting in constructing functional organs.
Topics: Humans; Tissue Engineering; Bioprinting; Printing, Three-Dimensional; Regenerative Medicine; Heart
PubMed: 37850299
DOI: 10.1039/d3tb01630g