Publisher: ASPET   (Total: 4 journals)   [Sort alphabetically]

Showing 1 - 4 of 4 Journals sorted by number of followers
Drug Metabolism and Disposition     Hybrid Journal   (Followers: 11, SJR: 1.433, CiteScore: 4)
J. of Pharmacology and Experimental Therapeutics     Hybrid Journal   (Followers: 9, SJR: 1.586, CiteScore: 4)
Molecular Pharmacology     Hybrid Journal   (Followers: 2, SJR: 2.076, CiteScore: 4)
Pharmacological Reviews     Hybrid Journal   (Followers: 1, SJR: 9.472, CiteScore: 20)
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Pharmacological Reviews
Journal Prestige (SJR): 9.472
Citation Impact (citeScore): 20
Number of Followers: 1  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Online) 1521-0081
Published by ASPET Homepage  [4 journals]
  • Sex/Gender Differences in the Time-Course for the Development of Substance
           Use Disorder: A Focus on the Telescoping Effect [Review Article]

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      Authors: Towers, E. B; Williams, I. L, Qillawala, E. I, Rissman, E. F, Lynch, W. J.
      Pages: 217 - 249
      Abstract: Sex/gender effects have been demonstrated for multiple aspects of addiction, with one of the most commonly cited examples being the "telescoping effect" where women meet criteria and/or seek treatment of substance use disorder (SUD) after fewer years of drug use as compared with men. This phenomenon has been reported for multiple drug classes including opioids, psychostimulants, alcohol, and cannabis, as well as nonpharmacological addictions, such as gambling. However, there are some inconsistent reports that show either no difference between men and women or opposite effects and a faster course to addiction in men than women. Thus, the goals of this review are to evaluate evidence for and against the telescoping effect in women and to determine the conditions/populations for which the telescoping effect is most relevant. We also discuss evidence from preclinical studies, which strongly support the validity of the telescoping effect and show that female animals develop addiction-like features (e.g., compulsive drug use, an enhanced motivation for the drug, and enhanced drug-craving/vulnerability to relapse) more readily than male animals. We also discuss biologic factors that may contribute to the telescoping effect, such as ovarian hormones, and its neurobiological basis focusing on the mesolimbic dopamine reward pathway and the corticomesolimbic glutamatergic pathway considering the critical roles these pathways play in the rewarding/reinforcing effects of addictive drugs and SUD. We conclude with future research directions, including intervention strategies to prevent the development of SUD in women.Significance StatementOne of the most widely cited gender/sex differences in substance use disorder (SUD) is the "telescoping effect," which reflects an accelerated course in women versus men for the development and/or seeking treatment for SUD. This review evaluates evidence for and against a telescoping effect drawing upon data from both clinical and preclinical studies. We also discuss the contribution of biological factors and underlying neurobiological mechanisms and highlight potential targets to prevent the development of SUD in women.
      PubDate: 2023-02-13T08:19:09-08:00
      DOI: 10.1124/pharmrev.121.000361
      Issue No: Vol. 75, No. 2 (2023)
       
  • Pharmacological Targeting of Mitochondria in Diabetic Kidney Disease
           [Review Article]

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      Authors: Cleveland, K. H; Schnellmann, R. G.
      Pages: 250 - 262
      Abstract: Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease (ESRD) in the United States and many other countries. DKD occurs through a variety of pathogenic processes that are in part driven by hyperglycemia and glomerular hypertension, leading to gradual loss of kidney function and eventually progressing to ESRD. In type 2 diabetes, chronic hyperglycemia and glomerular hyperfiltration leads to glomerular and proximal tubular dysfunction. Simultaneously, mitochondrial dysfunction occurs in the early stages of hyperglycemia and has been identified as a key event in the development of DKD. Clinical management for DKD relies primarily on blood pressure and glycemic control through the use of numerous therapeutics that slow disease progression. Because mitochondrial function is key for renal health over time, therapeutics that improve mitochondrial function could be of value in different renal diseases. Increasing evidence supports the idea that targeting aspects of mitochondrial dysfunction, such as mitochondrial biogenesis and dynamics, restores mitochondrial function and improves renal function in DKD. We will review mitochondrial function in DKD and the effects of current and experimental therapeutics on mitochondrial biogenesis and homeostasis in DKD over time.Significance StatementDiabetic kidney disease (DKD) affects 20% to 40% of patients with diabetes and has limited treatment options. Mitochondrial dysfunction has been identified as a key event in the progression of DKD, and pharmacologically restoring mitochondrial function in the early stages of DKD may be a potential therapeutic strategy in preventing disease progression.
      PubDate: 2023-02-13T08:19:09-08:00
      DOI: 10.1124/pharmrev.122.000560
      Issue No: Vol. 75, No. 2 (2023)
       
  • Molecular Tweezers: Supramolecular Hosts with Broad-Spectrum Biological
           Applications [Review Article]

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      Authors: Shahpasand-Kroner, H; Siddique, I, Malik, R, Linares, G. R, Ivanova, M. I, Ichida, J, Weil, T, Münch, J, Sanchez-Garcia, E, Klärner, F.-G, Schrader, T, Bitan, G.
      Pages: 263 - 308
      Abstract: Lysine-selective molecular tweezers (MTs) are supramolecular host molecules displaying a remarkably broad spectrum of biologic activities. MTs act as inhibitors of the self-assembly and toxicity of amyloidogenic proteins using a unique mechanism. They destroy viral membranes and inhibit infection by enveloped viruses, such as HIV-1 and SARS-CoV-2, by mechanisms unrelated to their action on protein self-assembly. They also disrupt biofilm of Gram-positive bacteria. The efficacy and safety of MTs have been demonstrated in vitro, in cell culture, and in vivo, suggesting that these versatile compounds are attractive therapeutic candidates for various diseases, infections, and injuries. A lead compound called CLR01 has been shown to inhibit the aggregation of various amyloidogenic proteins, facilitate their clearance in vivo, prevent infection by multiple viruses, display potent anti-biofilm activity, and have a high safety margin in animal models. The inhibitory effect of CLR01 against amyloidogenic proteins is highly specific to abnormal self-assembly of amyloidogenic proteins with no disruption of normal mammalian biologic processes at the doses needed for inhibition. Therapeutic effects of CLR01 have been demonstrated in animal models of proteinopathies, lysosomal-storage diseases, and spinal-cord injury. Here we review the activity and mechanisms of action of these intriguing compounds and discuss future research directions.Significance StatementMolecular tweezers are supramolecular host molecules with broad biological applications, including inhibition of abnormal protein aggregation, facilitation of lysosomal clearance of toxic aggregates, disruption of viral membranes, and interference of biofilm formation by Gram-positive bacteria. This review discusses the molecular and cellular mechanisms of action of the molecular tweezers, including the discovery of distinct mechanisms acting in vitro and in vivo, and the application of these compounds in multiple preclinical disease models.
      PubDate: 2023-02-13T08:19:09-08:00
      DOI: 10.1124/pharmrev.122.000654
      Issue No: Vol. 75, No. 2 (2023)
       
  • Newly Developed Targeted Therapies Against the Androgen Receptor in
           Triple-Negative Breast Cancer: A Review [Review Article]

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      Authors: Choupani, E; Mahmoudi Gomari, M, Zanganeh, S, Nasseri, S, Haji-allahverdipoor, K, Rostami, N, Hernandez, Y, Najafi, S, Saraygord-Afshari, N, Hosseini, A.
      Pages: 309 - 327
      Abstract: Among different types of breast cancers (BC), triple-negative BC (TNBC) amounts to 15% to 20% of breast malignancies. Three principal characteristics of TNBC cells are (i) extreme aggressiveness, (ii) absence of hormones, and (iii) growth factor receptors. Due to the lack or poor expression of the estrogen receptor, human epidermal growth factor receptor 2, and progesterone receptor, TNBC is resistant to hormones and endocrine therapies. Consequently, chemotherapy is currently used as the primary approach against TNBC. Expression of androgen receptor (AR) in carcinoma cells has been observed in a subset of patients with TNBC; therefore, inhibiting androgen signaling pathways holds promise for TNBC targeting. The new AR inhibitors have opened up new therapy possibilities for BC patients carrying AR-positive TNBC cells. Our group provides a comprehensive review of the structure and function of the AR and clinical evidence for targeting the cell’s nuclear receptor in TNBC. We updated AR agonists, inhibitors, and antagonists. We also presented a new era of genetic manipulating CRISPR/Cas9 and nanotechnology as state-of-the-art approaches against AR to promote the efficiency of targeted therapy in TNBC.Significance StatementThe lack of effective treatment for triple-negative breast cancer is a health challenge. The main disadvantages of existing treatments are their side effects, due to their nonspecific targeting. Molecular targeting of cellular receptors, such as androgen receptors, increased expression in malignant tissues, significantly improving the survival rate of breast cancer patients.
      PubDate: 2023-02-13T08:19:09-08:00
      DOI: 10.1124/pharmrev.122.000665
      Issue No: Vol. 75, No. 2 (2023)
       
  • Pharmacology of Heparin and Related Drugs: An Update [Review Article]

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      Authors: Hogwood, J; Mulloy, B, Lever, R, Gray, E, Page, C. P.
      Pages: 328 - 379
      Abstract: Heparin has been used extensively as an antithrombotic and anticoagulant for close to 100 years. This anticoagulant activity is attributed mainly to the pentasaccharide sequence, which potentiates the inhibitory action of antithrombin, a major inhibitor of the coagulation cascade. More recently it has been elucidated that heparin exhibits anti-inflammatory effect via interference of the formation of neutrophil extracellular traps and this may also contribute to heparin's antithrombotic activity. This illustrates that heparin interacts with a broad range of biomolecules, exerting both anticoagulant and nonanticoagulant actions. Since our previous review, there has been an increased interest in these nonanticoagulant effects of heparin, with the beneficial role in patients infected with SARS2-coronavirus a highly topical example. This article provides an update on our previous review with more recent developments and observations made for these novel uses of heparin and an overview of the development status of heparin-based drugs.Significance StatementThis state-of-the-art review covers recent developments in the use of heparin and heparin-like materials as anticoagulant, now including immunothrombosis observations, and as nonanticoagulant including a role in the treatment of SARS-coronavirus and inflammatory conditions.
      PubDate: 2023-02-20T10:33:38-08:00
      DOI: 10.1124/pharmrev.122.000684
      Issue No: Vol. 75, No. 2 (2023)
       
  • Targeting Persistent Changes in Neuroimmune and Epigenetic Signaling in
           Adolescent Drinking to Treat Alcohol Use Disorder in Adulthood [Review
           Article]

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      Authors: Crews, F. T; Coleman, L. G, Macht, V. A, Vetreno, R. P.
      Pages: 380 - 396
      Abstract: Studies universally find early age of drinking onset is linked to lifelong risks of alcohol problems and alcohol use disorder (AUD). Assessment of the lasting effect of drinking during adolescent development in humans is confounded by the diversity of environmental and genetic factors that affect adolescent development, including emerging personality disorders and progressive increases in drinking trajectories into adulthood. Preclinical studies using an adolescent intermittent ethanol (AIE) exposure rat model of underage binge drinking avoid the human confounds and support lifelong changes that increase risks. AIE increases adult alcohol drinking, risky decision-making, reward-seeking, and anxiety as well as reductions in executive function that all increase risks for the development of an AUD. AIE causes persistent increases in brain neuroimmune signaling high-mobility group box 1 (HMGB1), Toll-like receptor, receptor for advanced glycation end products, and innate immune genes that are also found to be increased in human AUD brain. HMGB1 is released from cells by ethanol, both free and within extracellular vesicles, that act on neurons and glia, shifting transcription and cellular phenotype. AIE-induced decreases in adult hippocampal neurogenesis and loss of basal forebrain cholinergic neurons are reviewed as examples of persistent AIE-induced pathology. Both are prevented and reversed by anti-inflammatory and epigenetic drugs. Findings suggest AIE-increased HMGB1 signaling induces the RE-1 silencing transcript blunting cholinergic gene expression, shifting neuronal phenotype. Inhibition of HMGB1 neuroimmune signaling, histone methylation enzymes, and galantamine, the cholinesterase inhibitor, both prevent and reverse AIE pathology. These findings provide new targets that may reverse AUD neuropathology as well as other brain diseases linked to neuroimmune signaling.Significance StatementAdolescent underage binge drinking studies find that earlier adolescent drinking is associated with lifelong alcohol problems including high levels of lifetime alcohol use disorder (AUD). Preclinical studies find the underage binge drinking adolescent intermittent ethanol (AIE) model causes lasting changes in adults that increase risks of developing adult alcohol problems. Loss of hippocampal neurogenesis and loss of basal forebrain cholinergic neurons provide examples of how AIE-induced epigenetic and neuroimmune signaling provide novel therapeutic targets for adult AUD.
      PubDate: 2023-02-13T08:19:09-08:00
      DOI: 10.1124/pharmrev.122.000710
      Issue No: Vol. 75, No. 2 (2023)
       
 
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