Poly (ADP-Ribose) polymerase 1 and parthanatos in neurological diseases: From pathogenesis to therapeutic opportunities

Xu, Xiaoxue; Sun, Bowen; Zhao, Chuansheng

doi:10.1016/j.nbd.2023.106314

Cited by 9 publications

(6 citation statements)

References 273 publications

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“…As a matter of fact, inhibition of PARP‐1 has been recognized as a beneficial strategy for epilepsy. 20 Small interfering RNA‐mediated PARP‐1 knockdown could effectively protect HT22 cells against glutamate‐induced toxic effects. 19 The neuroprotective effect of TRPM2 knockout could decrease neuronal apoptosis via PARP‐1/BNIP3/AIF in epilepsy.…”

Section: Discussionmentioning

confidence: 99%

“…As a key opportunity to inhibit the occurrence of parthanatos, blocking the translocation of AIF from the mitochondria to the nucleus might improve neuronal degeneration in epilepsy. 20 , 21 Moreover, previous research has found that AIF knockout led to aberrant NSC proliferation and defective neuronal differentiation. 22 Given the shared protective neuronal function and mitochondrial location of SV2A and AIF, we hypothesized that SV2A can alleviate recurrent seizures of PRE by inhibiting parthanatos via interacting with AIF.…”

Section: Introductionmentioning

confidence: 99%

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Synaptic vesicle protein 2A mitigates parthanatos via apoptosis‐inducing factor in a rat model of pharmacoresistant epilepsy

Li,

Wang,

Ren

et al. 2024

CNS Neurosci Ther

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AimsSynaptic vesicle protein 2A (SV2A) is a unique therapeutic target for pharmacoresistant epilepsy (PRE). As seizure‐induced neuronal programmed death, parthanatos was rarely reported in PRE. Apoptosis‐inducing factor (AIF), which has been implicated in parthanatos, shares a common cytoprotective function with SV2A. We aimed to investigate whether parthanatos participates in PRE and is mitigated by SV2A via AIF.MethodsAn intraperitoneal injection of lithium chloride‐pilocarpine was used to establish an epileptic rat model, and phenytoin and phenobarbital sodium were utilized to select PRE and pharmacosensitive rats. The expression of SV2A was manipulated via lentivirus delivery into the hippocampus. Video surveillance was used to assess epileptic ethology. Biochemical tests were employed to test hippocampal tissues following a successful SV2A infection. Molecular dynamic calculations were used to simulate the interaction between SV2A and AIF.ResultsParthanatos core index, PARP1, PAR, nuclear AIF and MIF, γ‐H2AX, and TUNEL staining were all increased in PRE. SV2A is bound to AIF to form a stable complex, successfully inhibiting AIF and MIF nuclear translocation and parthanatos and consequently mitigating spontaneous recurrent seizures in PRE. Moreover, parthanatos deteriorated after the SV2A reduction.SignificanceSV2A protected hippocampal neurons and mitigated epileptic seizures by inhibiting parthanatos via binding to AIF in PRE.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Synaptic vesicle protein 2A mitigates parthanatos via apoptosis‐inducing factor in a rat model of pharmacoresistant epilepsy

Li,

Wang,

Ren

et al. 2024

CNS Neurosci Ther

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“…For example, chaperone-mediated autophagy can inhibit cardiomyocyte apoptosis induced by oxidative stress by inhibiting cleaved PARP1 protein expression ( 55 ); aurora kinase A knockdown promotes apoptosis in Epstein-Barr virus-infected atypical glandular cells through cleavage of caspase-3 and −9, and PARP1 ( 56 ). Additionally, the colocalization of PARP-1/AIF in the nucleus indicates that PARP-1 plays a pivotal role in AIF-mediated carbon ion pro-apoptosis ( 14 ). Therefore, it is hypothesized that RJNTF may exert an inhibitory effect on chondrocyte apoptosis through regulation of the PARP1/AIF pathway, and the subsequent experiments were designed to test this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

“…When the number of chondrocytes decreases, for example due to autophagy, senescence and apoptosis, the structure and the function of the cartilage are affected ( 7 – 10 ). Poly [ADP-ribose] polymerase-1 (PARP-1)-dependent cell death, known as parthanatos, ( 11 – 13 ) is caused by the overactivation of PARP1, which catalyzes the catabolism of intracellular nicotinamide adenine dinucleotide (NAD) to produce poly [ADP-ribose] (PAR), which is translocated to the cytoplasm and binds to the outer surface of the mitochondria, causing the release of apoptosis-inducing factor (AIF) and the recruitment of macrophage migration inhibitory factor (MIF) to the nucleus, where it acts as a DNA endonuclease in synergy with nucleic acid exonuclease G to induce chromatin condensation and DNA breaks, generating fragments ~50 kb in length and inducing apoptosis in parthanatos ( 12 , 14 , 15 ). No research has revealed the association of PARP1/AIF with chondrocyte apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Network pharmacology combined with experimental validation to investigate the effect of Rongjin Niantong Fang on chondrocyte apoptosis in knee osteoarthritis

Chen,

Zhang,

Luo

et al. 2024

Mol Med Rep

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Knee osteoarthritis (KOA) is a chronic degenerative disease that affects the quality of life of middle-aged and elderly individuals, and is one of the major factors leading to disability. Rongjin Niantong Fang (RJNTF) can alleviate the clinical symptoms of patients with KOA, but the molecular mechanism underlying its beneficial effects on KOA remains unknown. Using pharmacological analysis and in vitro experiments, the active components of RJNTF were analyzed to explore their potential therapeutic targets and mechanisms in KOA. The potential targets and core signaling pathways by which RJNTF exerts its effects on KOA were obtained from databases such as Gene Expression Omnibus, Traditional Chinese Medicine Systems Pharmacology and Analysis Platform. Subsequently, chondrocyte apoptosis was modeled using hydrogen peroxide (H 2 O 2 ). Cell Counting Kit-8 assay involving a poly [ADP-ribose] polymerase-1 (PARP1) inhibitor, DAPI staining, reverse transcription-quantitative PCR, Annexin V-FITC/PI staining and flow cytometry, western blotting and co-immunoprecipitation analysis were used to determine the therapeutic efficacy of RJNTF on KOA and to uncover the molecular mechanism. It was found that PARP1-knockdown lentivirus, incubation with PARP1 inhibitor PJ34, medium and high doses of RJNTF significantly reduced H 2 O 2 -induced chondrocyte apoptosis. Medium and high doses of RJNTF downregulated the expression of cleaved caspase-3, cleaved PARP1 and PAR total proteins, as well as nucleus proteins of apoptosis-inducing factor (AIF) and migration inhibitory factor (MIF), and upregulated the expression of caspase-3, PARP1 total protein, as well as the cytoplasmic expression of AIF and MIF, suggesting that RJNTF may inhibit chondrocyte apoptosis through the PARP1/AIF signaling pathway.

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“…Phytochemicals present in this plant includes tannic acid, oleanolic acid, uzarigenin, neriodorein, oleandrose, karabin, neriodin, nerium D, nerium F, oleanolic acid, digitoxigenin, gitoxigenin, neriantin, odoroside, adyresin, ursolic acid, oleandrin, scopolin, scopoletin, oleandrigenin, 16-acetyl gitoxigenin, deacetyloleandrin, and dambonitol. 49 The cardioprotective efficacy of NO flowers was investigated by Gayathri et al50, who used isoproterenol to induce myocardial oxidative stress in rats. [20]…”

Section: Nerium Oleandermentioning

confidence: 99%

Plant & its Bioactive Components Uses in Cardio-Potential Diseases: A Sectional Study for Different Herbs

Kumar,

Sood,

Nirala

et al. 2023

J. Res. Appl. Sci. Biotechnol.

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Thirty percent of all deaths that occur each year can be attributed to heart disease, stroke, and other forms of cardiovascular disease. The World Health Organisation (WHO) predicts that by the year 2030, the annual death toll from cardiovascular diseases will have increased to 22.2 million, up from the present annual total of 17.9 million. Mortality rates tend to go up in populations as they get older. The chance of dying from cardiovascular disease is significantly higher for females (51%) than it is for males (42%). The majority of people treat and prevent cardiovascular disease by using plant-based medications (also known as phytochemicals), either in addition to or in instead of pharmaceuticals that are readily available on the market. In this study, the efficacy of treating cardiovascular illness is evaluated using 92 different plants, including 15 terrestrial plants. A number of different medicinal herbs, including Daucus carota, Nerium oleander, Amaranthus Viridis, Ginkgo biloba, Terminalia arjuna, Picrorhiza kurroa, Salvia miltiorrhiza, Tinospora cordifolia, Mucuna pruriens, Hydrocotyle asiatica, Bombax ceiba, and Andrographis paniculate, are utilised to treat cardiovascular disease. There are a variety of active phytochemicals found in these plants, some of which include flavonoids, polyphenols, plant sterols, plant sulphur compounds, and terpenoids. Flavonoids, in general, are known to increase vasodilation by inhibiting the oxidation of low-density lipoprotein (LDL). Plant sterols reduce the amount of cholesterol in the blood, which in turn protects against cardiovascular disease. Plant sulphur compounds protect against cardiovascular disease in addition to their role in the activation of nuclear factor-erythroid factor 2-related factor 2 (Nrf2) and the inhibition of cholesterol formation. The incidence of cardiovascular disease can be reduced by increasing the synthesis of ATP in mitochondria, and terpenoids can diminish atherosclerotic lesion in the aortic valve. Even though several physiologically active compounds with acknowledged biological functions have been found in a wide variety of plants, the prevalence of cardiovascular disease continues to rise, making it imperative that effective CVD prevention and treatment strategies be developed. More research is required to understand both the mechanism and the individual phytochemicals in plants that treat CVD. GRAPHICAL ABSTRACT

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Poly (ADP-Ribose) polymerase 1 and parthanatos in neurological diseases: From pathogenesis to therapeutic opportunities

Cited by 9 publications

References 273 publications

Synaptic vesicle protein 2A mitigates parthanatos via apoptosis‐inducing factor in a rat model of pharmacoresistant epilepsy

Synaptic vesicle protein 2A mitigates parthanatos via apoptosis‐inducing factor in a rat model of pharmacoresistant epilepsy

Network pharmacology combined with experimental validation to investigate the effect of Rongjin Niantong Fang on chondrocyte apoptosis in knee osteoarthritis

Plant & its Bioactive Components Uses in Cardio-Potential Diseases: A Sectional Study for Different Herbs

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