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Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism

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A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 40618

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Special Issue Editors

Dr. Huashan Shi

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Guest Editor

1. State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, China
2. Collaborative Innovation Center for Biotherapy, Chengdu 610041, China
Interests: cancer vaccines; bioinformatics; clinical research; chemotherapy; tumor metastasis

Prof. Dr. Vishwanath Venketaraman

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Guest Editor

Microbiology/Immunology Department of Basic Medical Sciences, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA 91766-1854, USA
Interests: mycobacterial diseases; tuberculosis; host immune responses; pathogenesis
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Dear Colleagues,

Immunologists have long been puzzled by the self-destructive nature of the inflammatory response. Inflammation can be elicited by various harmful stimuli, such as microbial/viral infections, allergic reactions, chemical insults, lipotoxicity, tissue damage, or other types of traumas. Breaking down damaged cells and converting them into various nutrients which are useful for tissue regeneration is among the most important functions of the human immune system in maintaining health. A localized inflammatory response is protective if the human immune system can effectively eliminate the harmful stimuli and initiate the healing process. Cell self-destruction (programmed cell death) includes phenomena of apoptosis, pyroptosis, necroptosis, necrosis and so on. Phagocytosis is employed to remove various cell debris produced by cell self-destruction and for conversion into nutrients. The immune system thus represents a powerful nutrient generator. At these moments, digestion and immunity are interrelated and integrated, playing the essential role of disease prevention and immunonutrition acquisition. In the event of microbial/viral infections, the nutritional flux produced by infected host cell self-destruction (inflammation) may be much greater than those produced by normal apoptosis, and may even be much greater than the nutrition provided by daily food intake. Thus, infection-induced inflammation may induce illness-associated anorexia to avoid overnutrition. When the nutrition generated by the degradation of infection-damaged cells exceeds the nutritional requirements of tissue regeneration, most excess nutrients will be converted into lipid intermediates. Lipid intermediates will invade healthy non-adipose tissue, leading to lipotoxicity and further tissue damage. In such a case, the main product (lipid intermediates) of the inflammatory response is also a strong harming stimulus for tissue/cell damage. This is amplified during the inflammatory response, forming a vicious cycle, making inflammatory response extremely destructive. The state of overnutrition will be exacerbated by the loss of lean body mass, coupled with excess lipid intermediate spillover into healthy tissues and organs, exacerbating the inflammatory response, which is characteristic of critically ill or injured patients and of most autoimmune diseases. In this Special Issue, original research articles and reviews are welcomed. Research areas may include (but are not limited to) the following: microbial-/viral infection-induced host cell self-destruction as immunonutrition; programmed cell death and nutrients generation; cell self-destruction in illness, transient over-nutrition, lipotoxicity and involuntary weight loss.

Dr. Huashan Shi
Prof. Dr. Vishwanath Venketaraman
Guest Editors

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Keywords

autoimmunity
cell self-destruction
infection
inflammation
immunonutrition
lipotoxicity
metabolism
programmed cell death

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Published Papers (14 papers)

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Editorial

Jump to: Research, Review

3 pages, 217 KiB

Open AccessEditorial

Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism

by Ligen Yu

Biology 2023, 12(7), 949; https://doi.org/10.3390/biology12070949 - 3 Jul 2023

Cited by 1 | Viewed by 4775

Abstract

The main purpose of this Special Issue is to provide readers with current understandings of the interactions and causal relations among injury stimuli (including microorganism infections), immune response and overnutrition/lipotoxicity in disease pathogenesis [...] Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

Research

Jump to: Editorial, Review

15 pages, 6950 KiB

Open AccessArticle

Etomoxir Sodium Salt Promotes Imidazole Ketone Erastin-Induced Myeloid-Derived Suppressor Cell Ferroptosis and Enhances Cancer Therapy

by Nada Mohamady Farouk Abdalsalam, Zihao Liang, Hafiza Kashaf Tariq, Abdulrahman Ibrahim, Rong Li, Xiaochun Wan and Dehong Yan

Biology 2024, 13(11), 949; https://doi.org/10.3390/biology13110949 - 19 Nov 2024

Viewed by 275

Abstract

Although ferroptosis inducers trigger ferroptotic tumor cells and immune cells in the tumor microenvironment (TME), imidazole ketone erastin (IKE)’s induction of ferroptosis shows no effect on tumor growth in immunocompetent tumor-bearing mice due to the presence of myeloid-derived suppressor cells (MDSCs). Treatment of the carnitine palmitoyltransferase 1a (CPT1A)-specific inhibitor decreases the immunosuppressive function of MDSCs and enhances ferroptotic inducer-initiated tumor cell ferroptosis. However, whether blocking CPT1A could enhance IKE-induced MDSC ferroptosis and thereby inhibit tumor growth is still unclear. Here, we report that a CPT1A-specific inhibitor, etomoxir sodium salt (Eto), and IKE combined treatment increased MDSC ferroptosis. Interestingly, the combination treatment of Eto and IKE blocked MDSCs’ immunosuppressive function and accumulation by downregulating the expression of SLC7A11, GPX4, and ARG1 while promoting T-cell proliferation and infiltration into tumor tissues to enhance cancer therapy. These data provide a rationale for the combination therapy of a specific CPT1A inhibitor, Eto, with IKE in clinical settings. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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14 pages, 3900 KiB

Open AccessArticle

Identification of Cuproptosis-Associated Prognostic Gene Expression Signatures from 20 Tumor Types

by Ednah Ooko, Nadeen T. Ali and Thomas Efferth

Biology 2024, 13(10), 793; https://doi.org/10.3390/biology13100793 - 3 Oct 2024

Viewed by 900

Abstract

We investigated the mRNA expression of 124 cuproptosis-associated genes in 7489 biopsies from 20 different tumor types of The Cancer Genome Atlas (TCGA). The KM plotter algorithm has been used to calculate Kaplan–Meier statistics and false discovery rate (FDR) corrections. Interaction networks have been generated using Ingenuity Pathway Analysis (IPA). High mRNA expression of 63 out of 124 genes significantly correlated with shorter survival times of cancer patients across all 20 tumor types. IPA analyses revealed that their gene products were interconnected in canonical pathways (e.g., cancer, cell death, cell cycle, cell signaling). Four tumor entities showed a higher accumulation of genes than the other cancer types, i.e., renal clear cell carcinoma (n = 21), renal papillary carcinoma (n = 13), kidney hepatocellular carcinoma (n = 13), and lung adenocarcinoma (n = 9). These gene clusters may serve as prognostic signatures for patient survival. These signatures were also of prognostic value for tumors with high mutational rates and neoantigen loads. Cuproptosis is of prognostic significance for the survival of cancer patients. The identification of specific gene signatures deserves further exploration for their clinical utility in routine diagnostics. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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13 pages, 2355 KiB

Open AccessArticle

Avian Coronavirus Infectious Bronchitis Virus Activates Mitochondria-Mediated Apoptosis Pathway and Affects Viral Replication by Inducing Reactive Oxygen Species Production in Chicken HD11 Cells

by Xiaoxiao Han, Yuan Huang and Junli Hao

Biology 2024, 13(7), 491; https://doi.org/10.3390/biology13070491 - 1 Jul 2024

Viewed by 1144

Abstract

Infectious bronchitis virus (IBV), a coronavirus that causes severe respiratory and gastrointestinal illness in poultry, leads to substantial economic losses. According to earlier research, IBV infection causes chicken macrophage HD11 cells to undergo cell apoptosis. Reactive oxygen species (ROS) and the IBV-activated intrinsic apoptotic signaling pathway were examined in this work. The findings demonstrate that IBV infection causes ROS to accumulate. Moreover, IBV infection decreased the mitochondrial transmembrane potential in HD11 cells, which could be blocked by ROS antioxidants (PDTC and NAC). The two antioxidants significantly affected the expression of Bcl-2 and Bax and further inhibited the activation of caspase-3 and apoptosis in HD11 cells. Additionally, IBV replication was decreased by blocking ROS accumulation. Pretreating HD11 cells with ammonium chloride (NH₄Cl) prevented IBV from entering the cells and reduced the oxidative stress which IBV causes. The ability to accumulate ROS was also lost in UV-inactivated IBV. The IBV N protein induces cell apoptosis through the activation of ROS. These findings provide an explanation for the processes of IBV infection in immune cells by indicating that IBV-induced ROS generation triggers cell apoptosis in HD11 cells. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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14 pages, 3119 KiB

Open AccessArticle

Protector Role of Cx30.2 in Pancreatic β-Cell against Glucotoxicity-Induced Apoptosis

by Daniel Ortega-Cuellar, Ignacio González-Sánchez, Gabriela Piñón-Zárate, Marco A. Cerbón, Víctor De la Rosa, Yuliana Franco-Juárez, Andrés Castell-Rodríguez, León D. Islas and Cristina Coronel-Cruz

Biology 2024, 13(7), 468; https://doi.org/10.3390/biology13070468 - 25 Jun 2024

Viewed by 1311

Abstract

Glucotoxicity may exert its deleterious effects on pancreatic β-cell function via a myriad of mechanisms, leading to impaired insulin secretion and, eventually, type 2 diabetes. β-cell communication requires gap junction channels to be present among these cells. Gap junctions are constituted by transmembrane proteins of the connexins (Cxs) family. Two Cx genes have been identified in β cells, Cx36 and Cx30.2. We have found evidence that the glucose concentration on its own is sufficient to regulate Cx30.2 gene expression in mouse islets. In this work, we examine the involvement of the Cx30.2 protein in the survival of β cells (RIN-m5F). Methods: RIN-m5F cells were cultured in 5 mM D-glucose (normal) or 30 mM D-glucose (high glucose) for 24 h. Cx30.2 siRNAs was used to downregulate Cx30.2 expression. Apoptosis was measured by means of TUNEL, an annexin V staining method, and the cleaved form of the caspase-3 protein was determined using Western blot. Results: High glucose did not induce apoptosis in RIN-m5F β cells after 24 h; interestingly, high glucose increased the Cx30.2 total protein levels. Moreover, this work found that the downregulation of Cx30.2 expression in high glucose promoted apoptosis in RIN-m5F cells. Conclusion: The data suggest that the upregulation of Cx30.2 protects β cells from hyperglycemia-induced apoptosis. Furthermore, Cx30.2 may be a promising avenue of therapeutic investigation for the treatment of glucose metabolic disorders. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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12 pages, 3999 KiB

Open AccessArticle

Modulation of Apoptosis by Bovine Gammaherpesvirus 4 Infection in Bovine Endometrial Cells and the Possible Role of LPS in This Process

by Florencia Romeo, Santiago Delgado, Marisol Yavorsky, Lucía Martinez Cuesta, Susana Pereyra, Erika González Altamiranda, Enrique Louge Uriarte, Sandra Pérez and Andrea Verna

Biology 2024, 13(4), 249; https://doi.org/10.3390/biology13040249 - 8 Apr 2024

Cited by 1 | Viewed by 1630

Abstract

The prevalent pathogens associated with bovine uterine infections are bacteria that appear to increase the host’s susceptibility to secondary infections with other bacteria or viruses, among which BoGHV4 is the most frequently found. In this work, the study of the pathways of apoptosis induction was carried out on an experimental model of primary culture of endometrial cells, in order to know the implication of BoGHV4 and the presence of bacterial LPS in the pathogenesis of the bovine reproductive tract. For this, different staining techniques and molecular analysis by RT-PCR were used. The results obtained allowed us to conclude that the level of cell death observed in the proposed primary culture is directly related to the time of viral infection and the presence of LPS in BoGHV4 infection. The apoptosis indices in cells infected with BoGHV4 and BoGHV4 + LPS revealed a maximum that correlated with the appearance of cytopathic effects and the maximum viral titers in the model studied. However, morphological, biochemical, and molecular changes were evident during both early and late stages of apoptosis. These findings provide information on the factors that may influence the pathogenesis of BoGHV4 and help to better understand the mechanisms involved in virus infection. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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Review

Jump to: Editorial, Research

11 pages, 279 KiB

Open AccessReview

Immunonutrition, Metabolism, and Programmed Cell Death in Lung Cancer: Translating Bench to Bedside

by Palma Fedele, Anna Natalizia Santoro, Francesca Pini, Marcello Pellegrino, Giuseppe Polito, Maria Chiara De Luca, Antonietta Pignatelli, Michele Tancredi, Valeria Lagattolla, Alessandro Anglani, Chiara Guarini, Antonello Pinto and Pietro Bracciale

Biology 2024, 13(6), 409; https://doi.org/10.3390/biology13060409 - 4 Jun 2024

Cited by 1 | Viewed by 1998

Abstract

Lung cancer presents significant therapeutic challenges, motivating the exploration of novel treatment strategies. Programmed cell death (PCD) mechanisms, encompassing apoptosis, autophagy, and programmed necrosis, are pivotal in lung cancer pathogenesis and the treatment response. Dysregulation of these pathways contributes to tumor progression and therapy resistance. Immunonutrition, employing specific nutrients to modulate immune function, and metabolic reprogramming, a hallmark of cancer cells, offer promising avenues for intervention. Nutritional interventions, such as omega-3 fatty acids, exert modulatory effects on PCD pathways in cancer cells, while targeting metabolic pathways implicated in apoptosis regulation represents a compelling therapeutic approach. Clinical evidence supports the role of immunonutritional interventions, including omega-3 fatty acids, in augmenting PCD and enhancing treatment outcomes in patients with lung cancer. Furthermore, synthetic analogs of natural compounds, such as resveratrol, demonstrate promising anticancer properties by modulating apoptotic signaling pathways. This review underscores the convergence of immunonutrition, metabolism, and PCD pathways in lung cancer biology, emphasizing the potential for therapeutic exploration in this complex disease. Further elucidation of the specific molecular mechanisms governing these interactions is imperative for translating these findings into clinical practice and improving lung cancer management. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

21 pages, 1440 KiB

Open AccessReview

Exercise-Mediated Protection against Air Pollution-Induced Immune Damage: Mechanisms, Challenges, and Future Directions

by Xingsheng Jin, Yang Chen, Bingxiang Xu and Haili Tian

Biology 2024, 13(4), 247; https://doi.org/10.3390/biology13040247 - 8 Apr 2024

Cited by 1 | Viewed by 2119

Abstract

Air pollution, a serious risk factor for human health, can lead to immune damage and various diseases. Long-term exposure to air pollutants can trigger oxidative stress and inflammatory responses (the main sources of immune impairment) in the body. Exercise has been shown to modulate anti-inflammatory and antioxidant statuses, enhance immune cell activity, as well as protect against immune damage caused by air pollution. However, the underlying mechanisms involved in the protective effects of exercise on pollutant-induced damage and the safe threshold for exercise in polluted environments remain elusive. In contrast to the extensive research on the pathogenesis of air pollution and the preventive role of exercise in enhancing fitness, investigations into exercise resistance to injury caused by air pollution are still in their infancy. In this review, we analyze evidence from humans, animals, and cell experiments on the combined effects of exercise and air pollution on immune health outcomes, with an emphasis on oxidative stress, inflammatory responses, and immune cells. We also propose possible mechanisms and directions for future research on exercise resistance to pollutant-induced damage in the body. Furthermore, we suggest strengthening epidemiological studies at different population levels and investigations on immune cells to guide how to determine the safety thresholds for exercise in polluted environments. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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25 pages, 2310 KiB

Open AccessReview

Overnutrition and Lipotoxicity: Impaired Efferocytosis and Chronic Inflammation as Precursors to Multifaceted Disease Pathogenesis

by Vivek Mann, Alamelu Sundaresan and Shishir Shishodia

Biology 2024, 13(4), 241; https://doi.org/10.3390/biology13040241 - 6 Apr 2024

Cited by 3 | Viewed by 2334

Abstract

Overnutrition, driven by the consumption of high-fat, high-sugar diets, has reached epidemic proportions and poses a significant global health challenge. Prolonged overnutrition leads to the deposition of excessive lipids in adipose and non-adipose tissues, a condition known as lipotoxicity. The intricate interplay between overnutrition-induced lipotoxicity and the immune system plays a pivotal role in the pathogenesis of various diseases. This review aims to elucidate the consequences of impaired efferocytosis, caused by lipotoxicity-poisoned macrophages, leading to chronic inflammation and the subsequent development of severe infectious diseases, autoimmunity, and cancer, as well as chronic pulmonary and cardiovascular diseases. Chronic overnutrition promotes adipose tissue expansion which induces cellular stress and inflammatory responses, contributing to insulin resistance, dyslipidemia, and metabolic syndrome. Moreover, sustained exposure to lipotoxicity impairs the efferocytic capacity of macrophages, compromising their ability to efficiently engulf and remove dead cells. The unresolved chronic inflammation perpetuates a pro-inflammatory microenvironment, exacerbating tissue damage and promoting the development of various diseases. The interaction between overnutrition, lipotoxicity, and impaired efferocytosis highlights a critical pathway through which chronic inflammation emerges, facilitating the development of severe infectious diseases, autoimmunity, cancer, and chronic pulmonary and cardiovascular diseases. Understanding these intricate connections sheds light on potential therapeutic avenues to mitigate the detrimental effects of overnutrition and lipotoxicity on immune function and tissue homeostasis, thereby paving the way for novel interventions aimed at reducing the burden of these multifaceted diseases on global health. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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50 pages, 2313 KiB

Open AccessReview

Exploring beyond Common Cell Death Pathways in Oral Cancer: A Systematic Review

by Leonardo de Oliveira Siquara da Rocha, Everton Freitas de Morais, Lilianny Querino Rocha de Oliveira, Andressa Vollono Barbosa, Daniel W. Lambert, Clarissa A. Gurgel Rocha and Ricardo D. Coletta

Biology 2024, 13(2), 103; https://doi.org/10.3390/biology13020103 - 6 Feb 2024

Cited by 3 | Viewed by 2626

Abstract

Oral squamous cell carcinoma (OSCC) is the most common and lethal type of head and neck cancer in the world. Variable response and acquisition of resistance to traditional therapies show that it is essential to develop novel strategies that can provide better outcomes for the patient. Understanding of cellular and molecular mechanisms of cell death control has increased rapidly in recent years. Activation of cell death pathways, such as the emerging forms of non-apoptotic programmed cell death, including ferroptosis, pyroptosis, necroptosis, NETosis, parthanatos, mitoptosis and paraptosis, may represent clinically relevant novel therapeutic opportunities. This systematic review summarizes the recently described forms of cell death in OSCC, highlighting their potential for informing diagnosis, prognosis and treatment. Original studies that explored any of the selected cell deaths in OSCC were included. Electronic search, study selection, data collection and risk of bias assessment tools were realized. The literature search was carried out in four databases, and the extracted data from 79 articles were categorized and grouped by type of cell death. Ferroptosis, pyroptosis, and necroptosis represented the main forms of cell death in the selected studies, with links to cancer immunity and inflammatory responses, progression and prognosis of OSCC. Harnessing the potential of these pathways may be useful in patient-specific prognosis and individualized therapy. We provide perspectives on how these different cell death types can be integrated to develop decision tools for diagnosis, prognosis, and treatment of OSCC. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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29 pages, 1744 KiB

Open AccessReview

Types of Cell Death from a Molecular Perspective

by Fatemeh Hajibabaie, Navid Abedpoor and Parisa Mohamadynejad

Biology 2023, 12(11), 1426; https://doi.org/10.3390/biology12111426 - 13 Nov 2023

Cited by 11 | Viewed by 4818

Abstract

The former conventional belief was that cell death resulted from either apoptosis or necrosis; however, in recent years, different pathways through which a cell can undergo cell death have been discovered. Various types of cell death are distinguished by specific morphological alterations in the cell’s structure, coupled with numerous biological activation processes. Various diseases, such as cancers, can occur due to the accumulation of damaged cells in the body caused by the dysregulation and failure of cell death. Thus, comprehending these cell death pathways is crucial for formulating effective therapeutic strategies. We focused on providing a comprehensive overview of the existing literature pertaining to various forms of cell death, encompassing apoptosis, anoikis, pyroptosis, NETosis, ferroptosis, autophagy, entosis, methuosis, paraptosis, mitoptosis, parthanatos, necroptosis, and necrosis. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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23 pages, 2999 KiB

Open AccessReview

Cellular Stress: Modulator of Regulated Cell Death

by Prem Prasad Lamichhane and Parimal Samir

Biology 2023, 12(9), 1172; https://doi.org/10.3390/biology12091172 - 25 Aug 2023

Cited by 5 | Viewed by 4284

Abstract

Cellular stress response activates a complex program of an adaptive response called integrated stress response (ISR) that can allow a cell to survive in the presence of stressors. ISR reprograms gene expression to increase the transcription and translation of stress response genes while repressing the translation of most proteins to reduce the metabolic burden. In some cases, ISR activation can lead to the assembly of a cytoplasmic membraneless compartment called stress granules (SGs). ISR and SGs can inhibit apoptosis, pyroptosis, and necroptosis, suggesting that they guard against uncontrolled regulated cell death (RCD) to promote organismal homeostasis. However, ISR and SGs also allow cancer cells to survive in stressful environments, including hypoxia and during chemotherapy. Therefore, there is a great need to understand the molecular mechanism of the crosstalk between ISR and RCD. This is an active area of research and is expected to be relevant to a range of human diseases. In this review, we provided an overview of the interplay between different cellular stress responses and RCD pathways and their modulation in health and disease. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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31 pages, 9155 KiB

Open AccessReview

The ACSL4 Network Regulates Cell Death and Autophagy in Diseases

by Fangquan Chen, Rui Kang, Jiao Liu and Daolin Tang

Biology 2023, 12(6), 864; https://doi.org/10.3390/biology12060864 - 15 Jun 2023

Cited by 12 | Viewed by 6165

Abstract

Lipid metabolism, cell death, and autophagy are interconnected processes in cells. Dysregulation of lipid metabolism can lead to cell death, such as via ferroptosis and apoptosis, while lipids also play a crucial role in the regulation of autophagosome formation. An increased autophagic response not only promotes cell survival but also causes cell death depending on the context, especially when selectively degrading antioxidant proteins or organelles that promote ferroptosis. ACSL4 is an enzyme that catalyzes the formation of long-chain acyl-CoA molecules, which are important intermediates in the biosynthesis of various types of lipids. ACSL4 is found in many tissues and is particularly abundant in the brain, liver, and adipose tissue. Dysregulation of ACSL4 is linked to a variety of diseases, including cancer, neurodegenerative disorders, cardiovascular disease, acute kidney injury, and metabolic disorders (such as obesity and non-alcoholic fatty liver disease). In this review, we introduce the structure, function, and regulation of ACSL4; discuss its role in apoptosis, ferroptosis, and autophagy; summarize its pathological function; and explore the potential implications of targeting ACSL4 in the treatment of various diseases. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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15 pages, 1228 KiB

Open AccessReview

New Perspectives on the Role of Nuclear Proteases in Cell Death Pathways

by Anastasia S. Frolova, Olga E. Chepikova, Anna S. Deviataikina, Alena D. Solonkina and Andrey A. Zamyatnin, Jr.

Biology 2023, 12(6), 797; https://doi.org/10.3390/biology12060797 - 31 May 2023

Cited by 3 | Viewed by 2520

Abstract

Multiple factors can trigger cell death via various pathways, and nuclear proteases have emerged as essential regulators of these processes. While certain nuclear proteases have been extensively studied and their mechanisms of action are well understood, others remain poorly characterized. Regulation of nuclear protease activity is a promising therapeutic strategy that could selectively induce favorable cell death pathways in specific tissues or organs. Thus, by understanding the roles of newly discovered or predicted nuclear proteases in cell death processes, we can identify new pharmacological targets for improving therapeutic outcomes. In this article, we delved into the role of nuclear proteases in several types of cell death and explore potential avenues for future research and therapeutic development. Full article

(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

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