scholarly journals The Function, Regulation and Mechanism of Programmed Cell Death of Macrophages in Atherosclerosis

2022 ◽  
Vol 9 ◽  
Author(s):  
Chang Liu ◽  
Zecheng Jiang ◽  
Zhongjie Pan ◽  
Liang Yang
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Cells ◽  
Critical Role ◽  
Inflammatory Cells ◽  
Cerebrovascular Diseases ◽  
Atherosclerotic Plaques ◽  
Whole Process ◽  
Programmed Death

Atherosclerosis is a chronic progressive inflammatory vascular disease, which is an important pathological basis for inducing a variety of cardio-cerebrovascular diseases. As a kind of inflammatory cells, macrophages are the most abundant immune cells in atherosclerotic plaques and participate in the whole process of atherosclerosis and are the most abundant immune cells in atherosclerotic plaques. Recent studies have shown that programmed cell death plays a critical role in the progression of many diseases. At present, it is generally believed that the programmed death of macrophages can affect the development and stability of atherosclerotic vulnerable plaques, and the intervention of macrophage death may become the target of atherosclerotic therapy. This article reviews the role of macrophage programmed cell death in the progression of atherosclerosis and the latest therapeutic strategies targeting macrophage death within plaques.

scholarly journals The Value of Programmed Death Ligand 1 Expression in Cancer Patients Treated with Neoadjuvant Chemotherapy

2019 ◽  
Vol 19 (4) ◽  
pp. 277 ◽  
Author(s):  
Malika Al-Dughaishi ◽  
Asem Shalaby ◽  
Khawla Al-Ribkhi ◽  
Ammar Boudaka ◽  
Mohamed-Rachid Boulassel ◽  
...  
Keyword(s):  
Cell Death ◽  
Neoadjuvant Chemotherapy ◽  
Programmed Cell Death ◽  
Cancer Patients ◽  
Cell Activity ◽  
Programmed Death Ligand 1 ◽  
Tumour Immunity ◽  
Programmed Death ◽  
Programmed Cell Death 1

Programmed death ligand 1 (PD-L1) is an inhibitory molecule expressed by cancer cells to supress T-cell activity and escape anti-tumour immunity. The role of PD-L1 in cancer has been studied extensively as it is considered an important immune checkpoint against immune over-activation through its interaction with Programmed death receptor 1 (PD-1) expressed on activated lymphocytes. PD-L1 expression was found to be enhanced by chemotherapy through different proliferation pathways. However, the predictive and prognostic value for PD-L1 expression in cancer patients treated with neoadjuvant chemotherapy (NAC) is not yet established. This review focused on the potential effects of chemotherapy on PD-L1 expression and the role of PD-L1 as a prognostic and predictive marker in NAC-treated cancer patients. In addition, the potential use of this marker in clinical practice is discussed.Keywords: Programmed Cell Death 1 Ligand 1; Programmed Cell Death 1 Receptor; Neoadjuvant Therapy; Cancer.

scholarly journals Programmed cell death recruits macrophages into the developing mouse cochlea

2021 ◽  
Author(s):  
Vikrant Borse ◽  
Tejbeer Kaur ◽  
Ashley Hinton ◽  
Kevin Ohlemiller ◽  
Mark E. Warchol
Keyword(s):  
Cell Death ◽  
Thyroid Hormone ◽  
Programmed Cell Death ◽  
Critical Role ◽  
Large Population ◽  
Developmental Time ◽  
Macrophage Recruitment ◽  
Time Period ◽  
Developmental Cell Death

AbstractProgrammed cell death (PCD) plays a critical role in the development and maturation of the cochlea. Significant remodeling occurs among cells of the greater epithelial ridge (GER) of Kölliker’s organ, leading to tissue regression and formation of the inner sulcus. In mice, this event normally occurs between postnatal days 5-15 (P5-15) and is regulated by thyroid hormone (T3). During this developmental time period, the cochlea also contains a large population of macrophages. Macrophages are frequently involved in the phagocytic clearance of dead cells, both during development and after injury, but the role of macrophages in the developing cochlea is unknown. This study examined the link between developmental cell death in the GER and the recruitment of macrophages into this region. Cell death in the basal GER begins at P5 and enhanced numbers of macrophages were observed at P7. This pattern of macrophage recruitment was unchanged in mice that were genetically deficient for CX3CR1, the receptor for fractalkine (a known macrophage chemoattractant). We found that injection of T3 at P0 and P1 caused GER cell death to begin at P3, and this premature PCD was accompanied by earlier recruitment of macrophages. We further found that depletion of macrophages from the developing cochlea (using CX3CR1DTR/+ mice and treatment with the CSF1R antagonist BLZ945) had no effects on the pattern of GER regression. Together, these findings suggest that macrophages are recruited into the GER region after initiation of developmental PCD, but that they are not essential for GER regression during cochlear remodeling.

scholarly journals Programmed Cell Death Recruits Macrophages Into the Developing Mouse Cochlea

2021 ◽  
Vol 9 ◽  
Author(s):  
Vikrant Borse ◽  
Tejbeer Kaur ◽  
Ashley Hinton ◽  
Kevin Ohlemiller ◽  
Mark E. Warchol
Keyword(s):  
Cell Death ◽  
Thyroid Hormone ◽  
Programmed Cell Death ◽  
Critical Role ◽  
Large Population ◽  
Developmental Time ◽  
Macrophage Recruitment ◽  
Time Period ◽  
Developmental Cell Death

Programmed cell death (PCD) plays a critical role in the development and maturation of the cochlea. Significant remodeling occurs among cells of the greater epithelial ridge (GER) of Kölliker’s organ, leading to tissue regression and formation of the inner sulcus. In mice, this event normally occurs between postnatal days 5–15 (P5-15) and is regulated by thyroid hormone (T3). During this developmental time period, the cochlea also contains a large population of macrophages. Macrophages are frequently involved in the phagocytic clearance of dead cells, both during development and after injury, but the role of macrophages in the developing cochlea is unknown. This study examined the link between developmental cell death in the GER and the recruitment of macrophages into this region. Cell death in the basal GER begins at P5 and enhanced numbers of macrophages were observed at P7. This pattern of macrophage recruitment was unchanged in mice that were genetically deficient for CX3CR1, the receptor for fractalkine (a known macrophage chemoattractant). We found that injection of T3 at P0 and P1 caused GER cell death to begin at P3, and this premature PCD was accompanied by earlier recruitment of macrophages. We further found that depletion of macrophages from the developing cochlea (using CX3CR1DTR/+ mice and treatment with the CSF1R antagonist BLZ945) had no effect on the pattern of GER regression. Together, these findings suggest that macrophages are recruited into the GER region after initiation of developmental PCD, but that they are not essential for GER regression during cochlear remodeling.

scholarly journals The prognostic role of immune checkpoint markers programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1) in a large, multicenter prostate cancer cohort

Oncotarget ◽  
2017 ◽  
Vol 8 (16) ◽  
pp. 26789-26801 ◽  
Author(s):  
Nora Ness ◽  
Sigve Andersen ◽  
Mehrdad Rakaee Khanehkenari ◽  
Cecilie V. Nordbakken ◽  
Andrej Valkov ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Checkpoint ◽  
Prognostic Role ◽  
Programmed Death Ligand 1 ◽  
Programmed Death ◽  
Cell Death Protein

scholarly journals Non-coding RNAs in necroptosis, pyroptosis and ferroptosis in cancer metastasis

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yan Liu ◽  
Qiuyun Chen ◽  
Yanan Zhu ◽  
Tiying Wang ◽  
Lijuan Ye ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Patients ◽  
Distant Metastasis ◽  
Tumor Metastasis ◽  
Cancer Metastasis ◽  
Non Coding Rna ◽  
Programmed Death ◽  
Non Coding Rnas

AbstractDistant metastasis is the main cause of death for cancer patients. Recently, the newly discovered programmed cell death includes necroptosis, pyroptosis, and ferroptosis, which possesses an important role in the process of tumor metastasis. At the same time, it is widely reported that non-coding RNA precisely regulates programmed death and tumor metastasis. In the present review, we summarize the function and role of necroptosis, pyrolysis, and ferroptosis involving in cancer metastasis, as well as the regulatory factors, including non-coding RNAs, of necroptosis, pyroptosis, and ferroptosis in the process of tumor metastasis.

scholarly journals Ferroptosis: New Dawn for Overcoming the Cardio-Cerebrovascular Diseases

2021 ◽  
Vol 9 ◽  
Author(s):  
Meng-Yi Luo ◽  
Jian-Hui Su ◽  
Shao-Xin Gong ◽  
Na Liang ◽  
Wen-Qian Huang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Ischemic Stroke ◽  
Dynamic Balance ◽  
Critical Role ◽  
Cerebrovascular Diseases ◽  
Regulatory Mechanisms ◽  
Prevention And Treatment ◽  
New Type

The dynamic balance of cardiomyocytes and neurons is essential to maintain the normal physiological functions of heart and brain. If excessive cells die in tissues, serious Cardio-Cerebrovascular Diseases would occur, namely, hypertension, myocardial infarction, and ischemic stroke. The regulation of cell death plays a role in promoting or alleviating Cardio-Cerebrovascular Diseases. Ferroptosis is an iron-dependent new type of cell death that has been proved to occur in a variety of diseases. In our review, we focus on the critical role of ferroptosis and its regulatory mechanisms involved in Cardio-Cerebrovascular Diseases, and discuss the important function of ferroptosis-related inhibitors in order to propose potential implications for the prevention and treatment of Cardio-Cerebrovascular Diseases.

The role of programmed cell death ligand-1/ programmed cell death-1 (PD-L1/PD-1) in HPV-induced cervical cancer and potential for their use in blockade therapy

2020 ◽  
Vol 27 ◽  
Author(s):  
Lifang Zhang ◽  
Yu Zhao ◽  
Quanmei Tu ◽  
Xiangyang Xue ◽  
Xueqiong Zhu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Escape ◽  
Hypoxia Inducible Factor ◽  
Hpv Infection ◽  
Advanced Cervical Cancer ◽  
Cervical Carcinogenesis ◽  
Programmed Cell Death 1

Background: Cervical cancer induced by infection with human papillomavirus (HPV) remains a leading cause of mortality for women worldwide although preventive vaccines and early diagnosis have reduced morbidity and mortality. Advanced cervical cancer can only be treated with either chemotherapy or radiotherapy but outcomes are poor. The median survival for advanced cervical cancer patients is only 16.8 months. Methods: We undertook a structural search of peer-reviewed published studies based on 1). Characteristics of programmed cell death ligand-1/programmed cell death-1(PD-L1/PD-1) expression in cervical cancer and upstream regulatory signals of PD-L1/PD-1 expression, 2). The role of the PD-L1/PD-1 axis in cervical carcinogenesis induced by HPV infection and 3). Whether the PD-L1/PD-1 axis has emerged as a potential target for cervical cancer therapies. Results: One hundred and twenty-six published papers were included in the review, demonstrating that expression of PD-L1/PD-1 is associated with HPV-caused cancer, especially with HPV 16 and 18 which account for approximately 70% of cervical cancer cases. HPV E5/E6/E7 oncogenes activate multiple signaling pathways including PI3K/AKT, MAPK, hypoxia-inducible factor 1α, STAT3/NF-kB and MicroRNAs, which regulate PD-L1/PD-1 axis to promote HPV-induced cervical carcinogenesis. The PD-L1/PD-1 axis plays a crucial role in immune escape of cervical cancer through inhibition of host immune response. creating an "immune-privileged" site for initial viral infection and subsequent adaptive immune resistance, which provides a rationale for therapeutic blockade of this axis in HPV-positive cancers. Currently, Phase I/II clinical trials evaluating the effects of PD-L1/PD-1 targeted therapies are in progress for cervical carcinoma, which provide an important opportunity for the application of anti-PD-L1/anti-PD-1 antibodies in cervical cancer treatment. Conclusion: Recent research developments have led to an entirely new class of drugs using antibodies against the PD-L1/PD-1 thus promoting the body’s immune system to fight the cancer. The expression and roles of the PD-L1/ PD-1 axis in the progression of cervical cancer provide great potential for using PD-L1/PD-1 antibodies as a targeted cancer therapy.

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