Poly (ADP-ribose) polymerase: An Overview of Mechanistic Approaches and Therapeutic Opportunities in the Management of Stroke

Tiwari, Palak; Khan, Heena; Singh, Thakur Gurjeet; Grewal, Amarjot Kaur

doi:10.1007/s11064-022-03595-z

Cited by 17 publications

(2 citation statements)

References 178 publications

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“…It can be activated by a single-strand DNA cleavage reaction, which may result from oxidative cell injury and the presence of free radicals. Mild activation of PARP (poly (ADP-ribose) polymerase) under physiological conditions regulates several cellular processes including DNA repair, gene expression, cell cycle progression, cell survival, chromatin remodeling, and maintenance of genomic stability 26 . However, excessive activation of PARP (poly (ADP-ribose) polymerase) leads to the depletion of cellular NAD + content 7 .…”

Section: The Relationship Between Nad + and Heart ...mentioning

confidence: 99%

NAD⁺-A Hub of Energy Metabolism in Heart Failure

Wu,

Pei,

2024

Int. J. Med. Sci.

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Heart failure is a condition where reduced levels of adenosine triphosphate (ATP) affect energy supply in myocardial cells. Nicotinamide adenine dinucleotide (NAD + ) plays a crucial role as a coenzyme for electron transfer in energy metabolism. Decreased NAD + levels in myocardial cells lead to inadequate ATP production and increased susceptibility to heart failure. Researchers are exploring ways to increase NAD + levels to alleviate heart failure. Targets such as sirtuin2 (sirt2), sirtuin3 (sirt3), Poly (ADP-ribose) polymerase (PARP), and diastolic regulatory proteins are being investigated. NAD + supplementation has shown promise, even in heart failure with preserved ejection fraction (HFpEF). By focusing on NAD + as a central component of energy metabolism, it is possible to improve myocardial activity, heart function, and address energy deficiency in heart failure.

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Section: The Relationship Between Nad + and Heart ...mentioning

confidence: 99%

NAD⁺-A Hub of Energy Metabolism in Heart Failure

Wu,

Pei,

2024

Int. J. Med. Sci.

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“…7 Many researchers have explored the efficacy and the underlying mechanisms of many drugs and treatment strategies for cerebral I/R injury. 8,9 Sevoflurane is the most commonly used anesthetic in clinical practice. In addition, it has been shown to have anti-inflammatory and neuroprotective activities.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane Postconditioning Attenuates Cerebral Ischemia-Reperfusion Injury by Inhibiting SP1/ACSL4-Mediated Ferroptosis

Lyu

2023

Hum Exp Toxicol

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Sevoflurane is the most commonly used anesthetic in clinical practice and exerts a protective effect on cerebral ischemia-reperfusion (I/R) injury. This study aims to elucidate the molecular mechanism by which sevoflurane postconditioning protects against cerebral I/R injury. Oxygen-glucose deprivation/reperfusion (OGD/R) model in vitro and the middle cerebral artery occlusion (MCAO) model in vivo were established to simulate cerebral I/R injury. Sevoflurane postconditioning reduced neurological deficits, cerebral infarction, and ferroptosis after I/R injury. Interestingly, sevoflurane significantly inhibited specificity protein 1 (SP1) expression in MACO rats and HT22 cells exposed to OGD/R. SP1 overexpression attenuated the neuroprotective effects of sevoflurane on OGD/R-treated HT22 cells, evidenced by reduced cell viability, increased apoptosis, and cleaved caspase-3 expression. Furthermore, chromatin immunoprecipitation and luciferase experiments verified that SP1 bound directly to the ACSL4 promoter region to increase its expression. In addition, sevoflurane inhibited ferroptosis via SP1/ACSL4 axis. Generally, our study describes an anti-ferroptosis effect of sevoflurane against cerebral I/R injury via downregulating the SP1/ASCL4 axis. These findings suggest a novel sight for cerebral protection against cerebral I/R injury and indicate a potential therapeutic approach for a variety of cerebral diseases.

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