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http://dx.doi.org/10.1016/j.yjmcc.2020.09.002 | DOI Listing |
Med Oncol
June 2024
Department of Biochemistry and Molecular Biology, University of Dhaka, Dhaka, 1000, Bangladesh.
Autophagy is a cytoplasmic defense mechanism that cells use to break and reprocess their intracellular components. This utilization of autophagy is regarded as a savior in nutrient-deficient and other stressful conditions. Hence, autophagy keeps contact with and responds to miscellaneous cellular tensions and diverse pathways of signal transductions, such as growth signaling and cellular death.
View Article and Find Full Text PDFJ Mol Cell Cardiol
November 2020
Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, La Jolla, CA, United States. Electronic address:
Toxicol Mech Methods
January 2017
a Department of Life Sciences , National Institute of Technology, Rourkela , India.
Polycyclic aromatic hydrocarbons (PAHs) comprise the major class of cancer-causing chemicals and are ranked ninth among the chemical compounds threatening to humans. Moreover, interest in PAHs has been mainly due to their genotoxic, teratogenic, mutagenic and carcinogenic property. Polymorphism in cytochrome P450 (CYP450) and aryl hydrocarbon receptor (AhR) has the capacity to convert procarcinogens into carcinogens, which is an imperative factor contributing to individual susceptibility to cancer development.
View Article and Find Full Text PDFAutophagy
November 2010
Department of Cardiology; Xijing Hospital; Fourth Military Medical University; Xi'an, China; Center for Cardiovascular Research and Alternative Medicine; University of Wyoming; Laramie, WY USA.
The mitochondrial isoform of aldehyde dehydrogenase (ALDH2) plays a key role in the metabolism of acetaldehyde and other toxic aldehydes. A recent seminal finding has indicated a potential role of ALDH2 activation in the cardioprotection against ischemic injury. Data from our group unveiled a myocardial protective effect of ALDH2 against ischemia/reperfusion (I/R) injury possibly through detoxification of toxic aldehydes: and a differential regulation of autophagy mediated by AMPK-mTOR and Akt-mTOR signaling cascades during ischemia and reperfusion, respectively.
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