Hongwei Shi's research while affiliated with Huazhong University of Science and Technology and other places
What is this page?
This page lists the scientific contributions of an author, who either does not have a ResearchGate profile, or has not yet added these contributions to their profile.
It was automatically created by ResearchGate to create a record of this author's body of work. We create such pages to advance our goal of creating and maintaining the most comprehensive scientific repository possible. In doing so, we process publicly available (personal) data relating to the author as a member of the scientific community.
If you're a ResearchGate member, you can follow this page to keep up with this author's work.
If you are this author, and you don't want us to display this page anymore, please let us know.
It was automatically created by ResearchGate to create a record of this author's body of work. We create such pages to advance our goal of creating and maintaining the most comprehensive scientific repository possible. In doing so, we process publicly available (personal) data relating to the author as a member of the scientific community.
If you're a ResearchGate member, you can follow this page to keep up with this author's work.
If you are this author, and you don't want us to display this page anymore, please let us know.
Publications (8)
Objectives:
Pirarubicin (THP) is widely used in clinical antitumor therapy, but its cardiotoxicity seriously affects the therapeutic effect in patients. In the study, we investigated the role of ring finger protein 10 (RNF10) in cardiotoxicity induced by THP.
Materials and methods:
A cardiac toxicity model in Sprague-Dawley (SD) rats induced by...
Pirarubicin (THP) is one of the classic chemotherapy drugs for cancer treatment. It is often clinically limited because of its cardiotoxicity. The occurrence and development of THP-mediated chemotherapy-related cardiotoxicity (CRC) may be reversed by RING finger protein 10 (RNF10). This study was performed with the aim of evaluating the inhibitory...
Objective:
Pirarubicin (THP) is one of anthracycline anticancer drugs. It is widely used in the treatment of various cancers, but its hepatotoxicity cannot be ignored. Schisandrin B (SchB) is a traditional liver-protecting drug, which has the ability to promote mitochondrial function and upregulate cellular antioxidant defense mechanism. However,...
[This corrects the article DOI: 10.3389/fphar.2021.733805.].
Objective: Pirarubicin (THP), one of the anthracycline anticancer drugs, is widely used in the treatment of various cancers, but its cardiotoxicity cannot be ignored. Schisandrin B (SchB) has the ability to upregulate cellular antioxidant defense mechanism and promote mitochondrial function and antioxidant status. However, it has not been reported...
Pirarubicin (THP), one of the anthracycline anticancer drugs, is widely used in the treatment of various types of cancer, but its cardiotoxicity cannot be ignored. Canagliflozin, the first sodium‑glucose co‑transporter‑2 inhibitor approved by the USA FDA, has been shown to have a significant effect on cardiovascular damage caused by diabetes. Howev...
Citations
... As a transcription factor, c-Jun, also called activator protein 1, plays a key role in the regulation of neuronal death and regeneration [8]. The JUN protein is believed to play a significant role in tumor development and occurrence, mainly regulating tumor cell survival and apoptosis [9][10][11]. The cells of glioblastomas were effectively killed by JUN-ELP-KLAK as demonstrated by Sarangthem et al. [12]. ...
... SOD and CAT protect cells from oxidative stress by detoxifying carcinogens or reducing stress; overproduction of ROS alters the oxidant-antioxidant balance. Excessive ROS disrupts the membrane lipid composition through lipid peroxidation, consequently increasing the levels of MDA, a final metabolite product of lipid peroxidation 22 . The peroxidation reaction increases free radical production, exacerbating cell damage. ...
... During ischemic stroke, brain tissue ischemia and hypoxia interfere with mitochondrial oxidative phosphorylation, leading to impaired energy metabolism and decreased ATP production. Tissue ATP is rapidly depleted and calcium ions (Ca 2+ ) are released from mitochondria and the endoplasmic reticulum [28]. This process produces free radicals that constrict large blood vessels, exacerbating ischemia and hypoxia and delaying recovery. ...
... Intracellularly, mitochondria play a vital role in oxidative phosphorylation, electron transportation and energy metabolism. After CI/R injury, mitochondria produce an excess of reactive oxygen species (ROS), leading to potential oxidative harm to the mitochondria (Orellana-Urzúa et al. 2020;Shi et al. 2021). This process may pry open the opening of the mitochondrial permeability transition pore (mPTP), triggering a decline in mitochondrial membrane potential (ΔΨm) and the release of cytochrome c (Cyt c) from the mitochondria (Chen et al. 2022). ...
... Однако похожее исследование, но уже с канаглифлозином, не подтвердило эффекта, наблюдаемого у эмпаглиф-лозина. Исследователи чётко установили, что канаглифлозин не оказывает существенного влияния на индуцированное поражение кардиомиоцитов [69]. ...