Background: Leishmania is a protozoan parasite that nests in macrophages and is responsible for the Leishmaniasis disease. In spite of different defense pathways, last strategy of macrophage for killing parasite is apoptosis process. By permeableizing the mitochondrial outer membrane (MOM). As breaching MOM releases apoptogenic factors like cytochrome-c which activate caspases that result in the destruction of the cell. In this review, we summarized the appropriate manuscripts regarding the bax includes, its different types and the effect of bax on the apoptosis of Leishmania and parasite-infected macrophages.
Methods: Information about the role of BAX in the apoptosis of parasite-infected macrophage of recent articles were surveyed by searching computerized bibliographic database PubMed and Google Scholar entering the keywords BAX and leishmaniasis.
Results: The common studies revealed Leishmania use different survival strategies for inhibiting macrophage apoptosis. As Leishmania by preventing homooligomerization or upregulating the anti-apoptotic molecule Bcl-2 can prohibits proteins of host-cell apoptosis such as Bax that is required for mitochondrial permeabilisation during apoptosis.
Conclusion: With regard to the supportive role of bax in apoptosis and the preventive role of Leishmania in its function, it seems that expression of bax gene in parasite by technologies like transgenic or down regulating of anti-apoptotic molecule Bcl-2 by miRNA could be prompted the apoptosis process of infected-macrophages and inhibited extensive spread of Leishmania and the resulting lesions.
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http://dx.doi.org/10.1016/j.micpath.2019.103892 | DOI Listing |
Discov Oncol
January 2025
Department of Biotechnology, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology (VIT), Vellore, 632014, India.
Cancer, one of the deadliest diseases, has remained the epicenter of biological research for more than seven decades. Yet all the efforts for a perfect therapeutic cure come with certain limitations. The use of medicinal plants and their phytochemicals as therapeutics has received much attention in recent years.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Molecular Genetics and Cancer Biology Laboratory, Department of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore-46, Tamil Nadu, India.
Background: Electromagnetic radiation (EMR) from wireless technology and mobile phones, operates at various frequencies. The present study analyses the major impact of short-term exposure to 2.4 GHz frequency EMR, using the two model systems chick embryos and SH-SY5Y cell lines.
View Article and Find Full Text PDFSleep Breath
January 2025
Nantong Key Laboratory of Translational Medicine in Cardiothoracic Diseases, and Research Institution of Translational Medicine in Cardiothoracic Diseases, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Background: Our previous study have demonstrated chronic intermittent hypoxia (CIH) induced cardiomyocyte apoptosis and cardiac dysfunction. However, the molecular mechanisms are complicated and varied. In this study, we first investigated the CaMKIIγ expression and signaling pathway in the pathogenesis of cardiomyocyte apoptosis after CIH.
View Article and Find Full Text PDFEur J Histochem
January 2025
Department of Critical Care Medicine, The Qujing No.1 People's Hospital, Qujing.
Intestinal barrier damage causes an imbalance in the intestinal flora and microbial environment, promoting a variety of gastrointestinal diseases. This study aimed to explore the mechanism by which adipose-derived stem cells (ADSCs) repair intestinal barrier damage. The human colon adenocarcinoma cell line Caco-2 and rats were treated with lipopolysaccharide (LPS) to establish in vitro and in vivo models, respectively, of intestinal barrier damage.
View Article and Find Full Text PDFRecent Pat Anticancer Drug Discov
January 2025
Department of Medical Oncology, Affiliated Hospital of Inner Mongolia Medical University, NO1 Tongdao Northern Road, Hohhot, 010050, China.
Background: Triple-negative breast cancer (TNBC) has a poor prognosis with current treatment options. Novel therapeutic strategies are urgently needed to enhance treatment outcomes for TNBC.
Objective: This study evaluated the efficacy of a three-agent regimen compared to existing treatment regimens in a TNBC mouse model, and elucidated its potential mechanisms of action.
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