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Cells Mar 2023Transcriptional regulation is fundamental to most biological processes and reverse-engineering programs can be used to decipher the underlying programs. In this review,... (Review)
Review
Transcriptional regulation is fundamental to most biological processes and reverse-engineering programs can be used to decipher the underlying programs. In this review, we describe how genomics is offering a systems biology-based perspective of the intricate and temporally coordinated transcriptional programs that control neuronal apoptosis and survival. In addition to providing a new standpoint in human pathology focused on the regulatory program, cracking the code of neuronal cell fate may offer innovative therapeutic approaches focused on downstream targets and regulatory networks. Similar to computers, where faults often arise from a software bug, neuronal fate may critically depend on its transcription program. Thus, cracking the code of neuronal life or death may help finding a patch for neurodegeneration and cancer.
Topics: Humans; Neurons; Gene Expression Regulation; Apoptosis; Cell Differentiation; Cell Death
PubMed: 37048129
DOI: 10.3390/cells12071057 -
International Journal of Biological... 2023Diabetic wounds are characterized by delayed and incomplete healing. As one of the most common complications of diabetes, diabetic wounds can be fatal in some cases.... (Review)
Review
Diabetic wounds are characterized by delayed and incomplete healing. As one of the most common complications of diabetes, diabetic wounds can be fatal in some cases. Programmed cell death (PCD) is an active and ordered cell death mode determined by genes, including apoptosis, autophagy, pyroptosis, necroptosis, ferroptosis, and cuproptosis. It is currently believed that PCD plays a crucial role in diabetic wound healing. Diabetic hyperglycemic environments can lead to abnormal PCD in various cells during healing processes, thereby affecting the activity and function of cells and interfering with diabetic wound healing. Therefore, this review focuses on the new roles and mechanisms of PCD in diabetic wound healing. Moreover, the challenges and perspectives related to PCD in diabetic wound healing are presented, which will bring new insights to improve diabetic wound healing.
Topics: Humans; Apoptosis; Cell Death; Diabetes Mellitus; Pyroptosis; Wound Healing
PubMed: 37781514
DOI: 10.7150/ijbs.88461 -
International Journal of Molecular... May 2023Apoptosis is a form of programmed cell death that is highly conserved in metazoan organisms, where it ensures the proper development and homeostasis of tissues [...].
Apoptosis is a form of programmed cell death that is highly conserved in metazoan organisms, where it ensures the proper development and homeostasis of tissues [...].
Topics: Animals; Proto-Oncogene Proteins c-bcl-2; bcl-X Protein; Apoptosis
PubMed: 37298435
DOI: 10.3390/ijms24119484 -
Journal of Translational Medicine Jul 2023Programmed cell death (PCD) plays an important role in many aspects of individual development, maintenance of body homeostasis and pathological processes. Ferroptosis is... (Review)
Review
Programmed cell death (PCD) plays an important role in many aspects of individual development, maintenance of body homeostasis and pathological processes. Ferroptosis is a novel form of PCD characterized by the accumulation of iron-dependent lipid peroxides resulting in lethal cell damage. It contributes to tumor progression in an apoptosis-independent manner. In recent years, an increasing number of non-coding RNAs (ncRNAs) have been demonstrated to mediate the biological process of ferroptosis, hence impacting carcinogenesis, progression, drug resistance, and prognosis. However, the clear regulatory mechanism for this phenomenon remains poorly understood. Moreover, ferroptosis does not usually exist independently. Its interaction with PCD, like apoptosis, necroptosis, autophagy, pyroptosis, and cuproptosis, to destroy cells appears to exist. Furthermore, ncRNA seems to be involved. Here, we review the mechanisms by which ferroptosis occurs, dissect its relationship with other forms of death, summarize the key regulatory roles played by ncRNAs, raise relevant questions and predict possible barriers to its application in the clinic, offering new ideas for targeted tumour therapy.
Topics: Humans; Ferroptosis; Apoptosis; Neoplasms; Carcinogenesis; Pyroptosis; RNA, Untranslated
PubMed: 37516888
DOI: 10.1186/s12967-023-04370-6 -
Frontiers in Immunology 2022Cell death is a necessary event in multi-cellular organisms to maintain homeostasis by eliminating unrequired or damaged cells. Currently, there are many forms of cell... (Review)
Review
Cell death is a necessary event in multi-cellular organisms to maintain homeostasis by eliminating unrequired or damaged cells. Currently, there are many forms of cell death, and several of them, such as necroptosis, pyroptosis and ferroptosis, even apoptosis trigger an inflammatory response by releasing damage-associated molecular patterns (DAMPs), which are involved in the pathogenesis of a variety of human inflammatory diseases, including autoimmunity disease, diabetes, Alzheimer's disease and cancer. Therefore, the occurrence of inflammatory cell death must be strictly regulated. Recently, increasing studies suggest that phosphorylation plays a critical role in inflammatory cell death. In this review, we will summarize current knowledge of the regulatory role of phosphorylation in inflammatory cell death and also discuss the promising treatment strategy for inflammatory diseases by targeting related protein kinases that mediate phosphorylation or phosphatases that mediate dephosphorylation.
Topics: Apoptosis; Cell Death; Humans; Necroptosis; Phosphorylation; Pyroptosis
PubMed: 35300338
DOI: 10.3389/fimmu.2022.851169 -
International Journal of Molecular... Dec 2016Programmed cell death is a vital biological process for multicellular organisms to maintain cellular homeostasis, which is regulated in a complex manner. Over the past... (Review)
Review
Programmed cell death is a vital biological process for multicellular organisms to maintain cellular homeostasis, which is regulated in a complex manner. Over the past several years, apart from apoptosis, which is the principal mechanism of caspase-dependent cell death, research on non-apoptotic forms of programmed cell death has gained momentum. p53 is a well characterized tumor suppressor that controls cell proliferation and apoptosis and has also been linked to non-apoptotic, non-canonical cell death mechanisms. p53 impacts these non-canonical forms of cell death through transcriptional regulation of its downstream targets, as well as direct interactions with key players involved in these mechanisms, in a cell type- or tissue context-dependent manner. In this review article, we summarize and discuss the involvement of p53 in several non-canonical modes of cell death, including caspase-independent apoptosis (CIA), ferroptosis, necroptosis, autophagic cell death, mitotic catastrophe, paraptosis, and pyroptosis, as well as its role in efferocytosis which is the process of clearing dead or dying cells.
Topics: Animals; Apoptosis; Autophagy; Cell Death; Humans; Necrosis; Pyroptosis; Signal Transduction; Tumor Suppressor Protein p53
PubMed: 27941671
DOI: 10.3390/ijms17122068 -
Cancer Biology & Therapy Sep 2016This review embarks upon a cell death journey from the discovery of apoptosis and necrosis through to the coalescence of these: necroptosis. The mechanisms of 2 emerging... (Review)
Review
This review embarks upon a cell death journey from the discovery of apoptosis and necrosis through to the coalescence of these: necroptosis. The mechanisms of 2 emerging necrotic cell death pathways, pyroptosis and ferroptosis, will be explored before delving into apoptotic and necroptotic signaling cascades, highlighting the complex interplay between molecular players. The involvement of the ripoptosome, interferon signaling and DNA damage in necroptosis will be discussed briefly. The major focus is on necroptosis initiation by tumor necrosis factor-α (TNFα) and its cognate receptor TNFR1, caspase-independent RIP1/RIP3/MLKL necrosome activation and cell death propagation by damage-associated molecular pattern (DAMP) release. Finally, the implications of a complex cell death signaling network will be revealed in the context of cancer biology and therapy. The clinical contribution of the discovery of necroptosis as an unequivocally new way of dying is monumental and could drastically alter cancer therapy strategies in the future.
Topics: Animals; Apoptosis; Cell Death; Humans; Necrosis
PubMed: 27434654
DOI: 10.1080/15384047.2016.1210732 -
International Urology and Nephrology May 2024Pyroptosis, a form of programmed cell death distinct from apoptosis and necrosis, is thought to be closely associated with the pathogenesis of diseases. Recently, the... (Review)
Review
Pyroptosis, a form of programmed cell death distinct from apoptosis and necrosis, is thought to be closely associated with the pathogenesis of diseases. Recently, the association between pyroptosis and urinary diseases has attracted considerable attention, and a comprehensive review focusing on this issue is not available. In this study, we reviewed the role of pyroptosis in the development and progression of benign urinary diseases and urinary malignancies. Based on this, pyroptosis has been implicated in the development of urinary diseases. In summary, this review sheds light on future research directions and provides novel ideas for using pyroptosis as a powerful tool to fight urinary diseases.
Topics: Humans; Pyroptosis; Urogenital Diseases; Apoptosis; Necrosis
PubMed: 38103146
DOI: 10.1007/s11255-023-03894-6 -
European Review For Medical and... Aug 2023Osteoarthritis (OA) is a high-incidence disease of the orthopedic system. However, studies on the molecular mechanisms of OA and pyroptosis, apoptosis, and necroptosis...
OBJECTIVE
Osteoarthritis (OA) is a high-incidence disease of the orthopedic system. However, studies on the molecular mechanisms of OA and pyroptosis, apoptosis, and necroptosis (PANoptosis) at the transcriptome level remain scarce. Therefore, this study purposed to detect biomarkers in OA and explore their relationship to the immune microenvironment.
MATERIALS AND METHODS
OA-related expression data was sourced from the Gene Expression Omnibus (GEO) database. Subsequently, differentially expressed analysis and a Venn diagram were performed to obtain differentially expressed PANoptosis-related genes (DEPGs). Furthermore, the least absolute shrinkage and selection operator (LASSO), Support Vector Machine-Recursive Feature Elimination (SVM-RFE), and random forest (RF) were implemented to screen diagnostic genes. Receiver operating characteristic (ROC) curves were performed to verify the diagnostic ability of the diagnostic genes. Next, immune infiltration analysis was performed to find the relationships between differential immune cells (OA vs. normal) and diagnostic genes. Finally, drug prediction analysis was also carried out, and the expression of diagnostic genes was verified in external datasets.
RESULTS
A total of 62 DEPGs were identified, which were enriched for regulating apoptotic signaling pathways, tumor necrosis factor (TNF) signaling pathways, and other related pathways. Three feature genes, nuclear factor-kappa-B inhibitor-alpha (NFKBIA), RING finger protein 34 (RNF34), and serine incorporator 3 (SERINC3) were obtained by intersecting genes obtained by the LASSO regression algorithm, SVM algorithm, and RF algorithm and showed excellent diagnostic efficacy with the Area under the curve (AUC) values of individual genes were all greater than 0.7, indicating that the model was more effective. Immuno-infiltration analysis showed that RNF34 was positively correlated with CD56dim natural killer cells, type 17 helper T cells, and NFKBIA was positively correlated with plasmacytoid dendritic cells. Additionally, 12 drugs were predicted by NFKBIA, such as gambogic acid and dioscin. In addition, NFKBIA and SERINC3 were significantly downregulated, and RNF34 was upregulated in OA samples.
CONCLUSIONS
Three genes (NFKBIA, RNF34, and SERINC3) related to PANoptosis, were obtained by bioinformatics analysis, which would provide a new direction for the diagnosis and treatment of OA.
Topics: Pyroptosis; Necroptosis; Apoptosis; Biomarkers; Algorithms
PubMed: 37667921
DOI: 10.26355/eurrev_202308_33396 -
Mediators of Inflammation 2018STING is a newly identified intracellular sensor of foreign and endogenous DNA. STING has been recognized as an activator of immune responses by TBK1/IRF3 and NF-B... (Review)
Review
STING is a newly identified intracellular sensor of foreign and endogenous DNA. STING has been recognized as an activator of immune responses by TBK1/IRF3 and NF-B pathways, and it is suggested to play critical roles in host defense, autoimmune diseases, and tumor immunity. Recent studies have revealed that the outcome of STING activation could vary between distinct cell types and scenarios. STING activation in certain cell types triggered cell death including apoptosis and necrosis. This effect could be critical for preventing unnecessary or excessive inflammatory events and maintaining host immune homeostasis. This review is dedicated to summarize recent evidences in the field of STING-mediated cell death and to demonstrate dual outcomes of STING signaling. Besides canonical immune responses represented by IFN and TNF productions, STING signaling can also induce cell death events in a variety of cell types. The double-faced characteristics of STING signaling requires further exploration and precious regulation before tailoring clinical strategies for associated diseases.
Topics: Animals; Apoptosis; Cell Death; Humans; Membrane Proteins; Necrosis; Signal Transduction
PubMed: 30595664
DOI: 10.1155/2018/1202797