The deletion of the gene coding for poly(ADP-ribose) polymerase-1 (PARP1) or its pharmacological inhibition protects mice against cerebral ischemia and Parkinson's disease. In sharp contrast, PARP1 inhibitors are in clinical use for the eradication of vulnerable cancer cells. It appears that excessive PARP1 activation is involved in a specific cell death pathway called parthanatos, while inhibition of PARP1 in cancer cells amplifies DNA damage to a lethal level. Hence, PARP1 plays a context-dependent role in cell fate decisions. In addition, it appears that PARP1 plays an ambiguous role in organismal aging.
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http://dx.doi.org/10.15698/cst2023.01.275 | DOI Listing |
Angew Chem Int Ed Engl
July 2024
MOE Key Laboratory of Bioinorganic and Synthetic Chemistry, State Key Laboratory of Anti-Infective Drug Discovery and Development, Guangdong Basic Research Center of Excellence for Functional Molecular Engineering, School of Chemistry, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510006, P. R. China.
Neurotherapeutics
October 2023
Graduate Programs in Neural and Behavioral Sciences, State University of New York Downstate Health Sciences University, 450 Clarkson Avenue, Brooklyn, New York, NY, 11203, USA.
Traumatic brain injury (TBI) results in both rapid and delayed brain damage. The speed, complexity, and persistence of TBI present large obstacles to drug development. Preclinical studies from multiple laboratories have tested the FDA-approved anti-microbial drug minocycline (MINO) to treat traumatic brain injury.
View Article and Find Full Text PDFApoptosis
April 2023
Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, School of Medicine, Northwest University, Taibai North Road 229, Xi'an, 710069, Shaanxi, China.
The normal colorectal mucosa undergoes precancerous lesions that can develop over time into colorectal cancer (CRC). In the stage of precancerous lesions, DNA replication stress may lead to genome instability. We have performed whole-exome sequencing on genomic DNA obtained from three cases of CRC tissues and identified a novel frameshift mutation of DNA damage inducible 1 homolog 2 gene (DDI2, c.
View Article and Find Full Text PDFFront Cell Dev Biol
May 2022
Department of General Surgery, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital of Capital Medical University, Beijing, China.
Barrett's esophagus is a major complication of gastro-esophageal reflux disease and an important precursor lesion for the development of Barrett's metaplasia and esophageal adenocarcinoma. However, the cellular and molecular mechanisms of Barrett's metaplasia remain unclear. Inflammation-associated oxidative DNA damage could contribute to Barrett's esophagus.
View Article and Find Full Text PDFNeural Regen Res
December 2022
Graduate Program in Neural and Behavioral Sciences; Department of Physiology and Pharmacology, State University of New York-Downstate Health Sciences University, Brooklyn, NY, USA.
Traumatic brain injury has a complex pathophysiology that produces both rapid and delayed brain damage. Rapid damage initiates immediately after injury. Treatment of traumatic brain injury is typically delayed many hours, thus only delayed damage can be targeted with drugs.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!