{"title":"Antioxidative properties of phenolic compounds and their effect on oxidative stress induced by severe physical exercise.","authors":"Joanna Kruk, Basil Hassan Aboul-Enein, Ewa Duchnik, Mariola Marchlewicz","doi":"10.1186/s12576-022-00845-1","DOIUrl":"10.1186/s12576-022-00845-1","url":null,"abstract":"<p><p>Extensive research has found strongly increased generation of reactive oxygen species, free radicals, and reactive nitrogen species during acute physical exercise that can lead to oxidative stress (OS) and impair muscle function. Polyphenols (PCs), the most abundant antioxidants in the human diet, are of increasing interest to athletes as antioxidants. Current literature suggests that antioxidants supplementation can effectively modulate these processes. This overview summarizes the actual knowledge of chemical and biomechanical properties of PCs and their impact as supplements on acute exercise-induced OS, inflammation control, and exercise performance. Evidence maintains that PC supplements have high potency to positively impact redox homeostasis and improve skeletal muscle's physiological and physical functions. However, many studies have failed to present improvement in physical performance. Eleven of 15 representative experimental studies reported a reduction of severe exercise-induced OS and inflammation markers or enhancement of total antioxidant capacity; four of eight studies found improvement in exercise performance outcomes. Further studies should be continued to address a safe, optimal PC dosage, supplementation timing during a severe training program in different sports disciplines, and effects on performance response and adaptations of skeletal muscle to exercise.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2022-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40605003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hypergravity load-induced hyperglycemia occurs due to hypothermia and increased plasma corticosterone level in mice.","authors":"Chikara Abe, Chikako Katayama, Kazuhiro Horii, Bakushi Ogawa, Kento Ohbayashi, Yusaku Iwasaki, Fumiaki Nin, Hironobu Morita","doi":"10.1186/s12576-022-00844-2","DOIUrl":"10.1186/s12576-022-00844-2","url":null,"abstract":"<p><p>Hypothermia has been observed during hypergravity load in mice and rats. This response is beneficial for maintaining blood glucose level, although food intake decreases. However, saving glucose is not enough to maintain blood glucose level during hypergravity load. In this study, we examined the contribution of humoral factors related to glycolysis in maintaining blood glucose level in a 2 G environment. Increased plasma corticosterone levels were observed in mice with intact peripheral vestibular organs, but not in mice with vestibular lesions. Plasma glucagon levels did not change, and decrease in plasma adrenaline levels was observed in mice with intact peripheral vestibular organs. Accordingly, it is possible that increase in plasma corticosterone level and hypothermia contribute to prevent hypoglycemia in a 2 G environment.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40674774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nelson Villalobos, Salvador Almazán-Alvarado, Victor Manuel Magdaleno-Madrigal
{"title":"Elevation of GABA levels in the globus pallidus disinhibits the thalamic reticular nucleus and desynchronized cortical beta oscillations.","authors":"Nelson Villalobos, Salvador Almazán-Alvarado, Victor Manuel Magdaleno-Madrigal","doi":"10.1186/s12576-022-00843-3","DOIUrl":"10.1186/s12576-022-00843-3","url":null,"abstract":"<p><p>The external globus pallidus (GP) is a GABAergic node involved in motor control regulation and coordinates firing and synchronization in the basal ganglia-thalamic-cortical network through inputs and electrical activity. In Parkinson's disease, high GABA levels alter electrical activity in the GP and contribute to motor symptoms. Under normal conditions, GABA levels are regulated by GABA transporters (GATs). GAT type 1 (GAT-1) is highly expressed in the GP, and pharmacological blockade of GAT-1 increases the duration of currents mediated by GABA A receptors and induces tonic inhibition. The functional contribution of the pathway between the GP and the reticular thalamic nucleus (RTn) is unknown. This pathway is important since the RTn controls the flow of information between the thalamus and cortex, suggesting that it contributes to cortical dynamics. In this work, we investigated the effect of increased GABA levels on electrical activity in the RTn by obtaining single-unit extracellular recordings from anesthetized rats and on the motor cortex (MCx) by corticography. Our results show that high GABA levels increase the spontaneous activity rate of RTn neurons and desynchronize oscillations in the beta frequency band in the MCx. Our findings provide evidence that the GP exerts tonic control over RTn activity through the GP-reticular pathway and functionally contributes to cortical oscillation dynamics.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2022-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40662117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shigehiko Ogoh, Takuro Washio, Benjamin S Stacey, Hayato Tsukamoto, Angelo Iannetelli, Thomas S Owens, Thomas A Calverley, Lewis Fall, Christopher J Marley, Damian M Bailey
{"title":"Effects of continuous hypoxia on flow-mediated dilation in the cerebral and systemic circulation: on the regulatory significance of shear rate phenotype.","authors":"Shigehiko Ogoh, Takuro Washio, Benjamin S Stacey, Hayato Tsukamoto, Angelo Iannetelli, Thomas S Owens, Thomas A Calverley, Lewis Fall, Christopher J Marley, Damian M Bailey","doi":"10.1186/s12576-022-00841-5","DOIUrl":"10.1186/s12576-022-00841-5","url":null,"abstract":"<p><p>Emergent evidence suggests that cyclic intermittent hypoxia increases cerebral arterial shear rate and endothelial function, whereas continuous exposure decreases anterior cerebral oxygen (O<sub>2</sub>) delivery. To examine to what extent continuous hypoxia impacts cerebral shear rate, cerebral endothelial function, and consequent cerebral O<sub>2</sub> delivery (CDO<sub>2</sub>), eight healthy males were randomly assigned single-blind to 7 h passive exposure to both normoxia (21% O<sub>2</sub>) and hypoxia (12% O<sub>2</sub>). Blood flow in the brachial and internal carotid arteries were determined using Duplex ultrasound and included the combined assessment of systemic and cerebral endothelium-dependent flow-mediated dilatation. Systemic (brachial artery) flow-mediated dilatation was consistently lower during hypoxia (P = 0.013 vs. normoxia), whereas cerebral flow-mediated dilation remained preserved (P = 0.927 vs. normoxia) despite a reduction in internal carotid artery antegrade shear rate (P = 0.002 vs. normoxia) and CDO<sub>2</sub> (P < 0.001 vs. normoxia). Collectively, these findings indicate that the reduction in CDO<sub>2</sub> appears to be independent of cerebral endothelial function and contrasts with that observed during cyclic intermittent hypoxia, highlighting the regulatory importance of (hypoxia) dose duration and flow/shear rate phenotype.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2022-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40610446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xin Yang, Heling Zhang, Tong Qu, Yi Wang, Yongxian Zhong, Yuchen Yan, Xuefei Ji, Tiayan Chi, Peng Liu, Libo Zou
{"title":"Tolfenamic acid inhibits ROS-generating oxidase Nox1-regulated p53 activity in intrastriatal injection of malonic acid rats.","authors":"Xin Yang, Heling Zhang, Tong Qu, Yi Wang, Yongxian Zhong, Yuchen Yan, Xuefei Ji, Tiayan Chi, Peng Liu, Libo Zou","doi":"10.1186/s12576-022-00842-4","DOIUrl":"10.1186/s12576-022-00842-4","url":null,"abstract":"<p><p>It has been reported that wild-type p53-induced gene 1 (Wig1), which is downstream of p53, regulates the expression of mutant huntingtin protein (mHtt) in Huntington's disease (HD) patients and transgenic mouse brains. Intrastriatal injection of malonic acid in rats is often used as a model to study the pathological changes of Huntington's disease, and this model has the advantages of a fast preparation and low cost. Therefore, in this study, we used intrastriatal injections of 6 μM malonic acid in rats to evaluate the effect of tolfenamic acid on motor and cognitive deficits and the effect of 6 mg/kg and 32 mg/kg tolfenamic acid on p53 and its downstream targets, such as Wig1. The results showed that 32 mg/kg tolfenamic acid attenuated motor and spatial memory dysfunction, prevented Nox1-mediated reactive oxygen species (ROS) production, and downregulated the activity of p53 by increasing the phosphorylation level at the Ser378 site and decreasing the acetylation level at the Lys382 site. Tolfenamic acid reduced mouse double minute 2 (Mdm2), phosphatase and tensin homologue (Pten), P53-upregulated modulator of apoptosis (Puma) and Bcl2-associated X (Bax) at the mRNA level to inhibit apoptosis and downregulated sestrin 2 (Sesn2) and hypoxia inducible factor 1, alpha subunit (Hif-1α) mRNA levels to exert antioxidative stress effects. In addition, 32 mg/kg tolfenamic acid played a role in neuroprotection by decreasing the terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL)-positive cell numbers. However, there was no difference in the Wig mRNA level among all groups, and tolfenamic acid could not decrease the protein level of Wig1. In conclusion, tolfenamic acid inhibited the ROS-generating oxidase Nox1-regulated p53 activity and attenuated motor and spatial memory deficits in malonic acid-injected rats.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2022-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40603348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of endurance training on metabolic enzyme activity and transporter protein levels in the skeletal muscles of orchiectomized mice.","authors":"Kenya Takahashi, Yu Kitaoka, Hideo Hatta","doi":"10.1186/s12576-022-00839-z","DOIUrl":"10.1186/s12576-022-00839-z","url":null,"abstract":"<p><p>This study investigated whether endurance training attenuates orchiectomy (ORX)-induced metabolic alterations. At 7 days of recovery after sham operation or ORX surgery, the mice were randomized to remain sedentary or undergo 5 weeks of treadmill running training (15-20 m/min, 60 min, 5 days/week). ORX decreased glycogen concentration in the gastrocnemius muscle, enhanced phosphofructokinase activity in the plantaris muscle, and decreased lactate dehydrogenase activity in the plantaris and soleus muscles. Mitochondrial enzyme activities and protein content in the plantaris and soleus muscles were also decreased after ORX, but preserved, in part, by endurance training. In the treadmill running test (15 m/min, 60 min) after 4 weeks of training, orchiectomized sedentary mice showed impaired exercise performance, which was restored by endurance training. Thus, endurance training could be a potential therapeutic strategy to prevent the hypoandrogenism-induced decline in muscle mitochondrial content and physical performance.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2022-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40409878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Early donepezil monotherapy or combination with metoprolol significantly prevents subsequent chronic heart failure in rats with reperfused myocardial infarction.","authors":"Meihua Li, Can Zheng, Toru Kawada, Kazunori Uemura, Masashi Inagaki, Keita Saku, Masaru Sugimachi","doi":"10.1186/s12576-022-00836-2","DOIUrl":"10.1186/s12576-022-00836-2","url":null,"abstract":"<p><p>Despite the presence of clinical guidelines recommending that β-blocker treatment be initiated early after reperfused myocardial infarction (RMI), acute myocardial infarction remains a leading cause of chronic heart failure (CHF). In this study, we compared the effects of donepezil, metoprolol, and their combination on the progression of cardiac remodeling in rats with RMI. The animals were randomly assigned to untreated (UT), donepezil-treated (DT), metoprolol-treated (MT), and a combination of donepezil and metoprolol (DMT) groups. On day 8 after surgery, compared to the UT, the DT and DMT significantly improved myocardial salvage, owing to the suppression of macrophage infiltration and apoptosis. After the 10-week treatment, the DT and DMT exhibited decreased heart rate, reduced myocardial infarct size, attenuated cardiac dysfunction, and decreased plasma levels of brain natriuretic peptide and catecholamine, thereby preventing subsequent CHF. These results suggest that donepezil monotherapy or combined therapy with β-blocker may be an alternative pharmacotherapy post-RMI.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2022-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40103813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Involvement of mechano-sensitive Piezo1 channel in the differentiation of brown adipocytes.","authors":"Manato Kenmochi, Satoko Kawarasaki, Satsuki Takizawa, Kazuhiko Okamura, Tsuyoshi Goto, Kunitoshi Uchida","doi":"10.1186/s12576-022-00837-1","DOIUrl":"10.1186/s12576-022-00837-1","url":null,"abstract":"<p><p>Brown adipocytes expend energy via heat production and are a potential target for the prevention of obesity and related metabolic disorders. Piezo1 is a Ca<sup>2+</sup>-permeable non-selective cation channel activated by mechanical stimuli. Piezo1 is reported to be involved in mechano-sensation in non-sensory tissues. However, the expression and roles of Piezo1 in brown adipocytes have not been well clarified. Here, we generated a brown adipocyte line derived from UCP1-mRFP1 transgenic mice and showed that Piezo1 is expressed in pre-adipocytes. Application of Yoda-1, a Piezo1 agonist, suppressed brown adipocyte differentiation, and this suppression was significantly attenuated by treatment with a Piezo1 antagonist and by Piezo1 knockdown. Furthermore, the suppression of brown adipocyte differentiation by Yoda-1 was abolished by co-treatment with a calcineurin inhibitor. Thus, these results suggest that activation of Piezo1 suppresses brown adipocyte differentiation via the calcineurin pathway.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2022-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717802/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40103731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Bicarbonate transport of airway surface epithelia in luminally perfused mice bronchioles.","authors":"Libin Liu, Akiko Yamamoto, Makoto Yamaguchi, Itsuka Taniguchi, Nao Nomura, Miyuki Nakakuki, Yuka Kozawa, Tomoya Fukuyasu, Mayuko Higuchi, Erina Niwa, Tsutomu Tamada, Hiroshi Ishiguro","doi":"10.1186/s12576-022-00828-2","DOIUrl":"10.1186/s12576-022-00828-2","url":null,"abstract":"<p><p>HCO<sub>3</sub><sup>-</sup> secretion in distal airways is critical for airway mucosal defense. HCO<sub>3</sub><sup>-</sup>/H<sup>+</sup> transport across the apical membrane of airway surface epithelial cells was studied by measuring intracellular pH in luminally microperfused freshly dissected mice bronchioles. Functional studies demonstrated that CFTR, ENaC, Cl<sup>-</sup>-HCO<sub>3</sub><sup>-</sup> exchange, Na<sup>+</sup>-H<sup>+</sup> exchange, and Na<sup>+</sup>-HCO<sub>3</sub><sup>-</sup> cotransport are involved in apical HCO<sub>3</sub><sup>-</sup>/H<sup>+</sup> transport. RT-PCR of isolated bronchioles detected fragments from Cftr, α, β, γ subunits of ENaC, Ae2, Ae3, NBCe1, NBCe2, NBCn1, NDCBE, NBCn2, Nhe1, Nhe2, Nhe4, Nhe5, Slc26a4, Slc26a6, and Slc26a9. We assume that continuous decline of intracellular pH following alkaline load demonstrates time course of HCO<sub>3</sub><sup>-</sup> secretion into the lumen which is perfused with a HCO<sub>3</sub><sup>-</sup>-free solution. Forskolin-stimulated HCO<sub>3</sub><sup>-</sup> secretion was substantially inhibited by luminal application of CFTR<sub>inh</sub>-172 (5 μM), H<sub>2</sub>DIDS (200 μM), and amiloride (1 μM). In bronchioles from a cystic fibrosis mouse model, basal and acetylcholine-stimulated HCO<sub>3</sub><sup>-</sup> secretion was substantially impaired, but forskolin transiently accelerated HCO<sub>3</sub><sup>-</sup> secretion of which the magnitude was comparable to wild-type bronchioles. In conclusion, we have characterized apical HCO<sub>3</sub><sup>-</sup>/H<sup>+</sup> transport in native bronchioles. We have demonstrated that cAMP-mediated and Ca<sup>2+</sup>-mediated pathways are involved in HCO<sub>3</sub><sup>-</sup> secretion and that apical HCO<sub>3</sub><sup>-</sup> secretion is largely mediated by CFTR and H<sub>2</sub>DIDS-sensitive Cl<sup>-</sup>-HCO<sub>3</sub><sup>-</sup> exchanger, most likely Slc26a9. The impairment of HCO<sub>3</sub><sup>-</sup> secretion in bronchioles from a cystic fibrosis mouse model may be related to the pathogenesis of early lung disease in cystic fibrosis.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2022-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39822506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Vidarabine, an anti-herpes agent, prevents occlusal-disharmony-induced cardiac dysfunction in mice.","authors":"Yoshio Hayakawa, Kenji Suita, Yoshiki Ohnuki, Yasumasa Mototani, Misao Ishikawa, Aiko Ito, Megumi Nariyama, Akinaka Morii, Kenichi Kiyomoto, Michinori Tsunoda, Ichiro Matsuo, Hiroshi Kawahara, Satoshi Okumura","doi":"10.1186/s12576-022-00826-4","DOIUrl":"10.1186/s12576-022-00826-4","url":null,"abstract":"<p><p>We recently reported a positive relationship between occlusal disharmony and cardiovascular disease via activation of β-adrenergic signaling in mice. Furthermore, inhibition of type 5 adenylyl cyclase (AC5), a major cardiac subtype in adults, protects the heart against oxidative stress. Here, we examined the role of AC5 in the development of occlusal-disharmony-induced cardiovascular disease in bite-opening (BO) mice, prepared by cementing a suitable appliance onto the mandibular incisor. We first examined the effects of BO treatment on cardiac function in mice treated or not treated for 2 weeks with vidarabine, which we previously identified as an inhibitor of cardiac AC. Cardiac function was significantly decreased in the BO group compared to the control group, but vidarabine ameliorated the dysfunction. Cardiac fibrosis, myocyte apoptosis and myocyte oxidative DNA damage were significantly increased in the BO group, but vidarabine blocked these changes. The BO-induced cardiac dysfunction was associated with increased phospholamban phosphorylation at threonine-17 and serine-16, as well as increased activation of the Ca<sup>2+</sup>-calmodulin-dependent protein kinase II/receptor-interacting protein 3 signaling pathway. These data suggest that AC5 inhibition with vidarabine might be a new therapeutic approach for the treatment of cardiovascular disease associated with occlusal disharmony.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2022-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39607217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}