chloroquine has been researched along with Atherogenesis in 12 studies
Chloroquine: The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses.
chloroquine : An aminoquinoline that is quinoline which is substituted at position 4 by a [5-(diethylamino)pentan-2-yl]amino group at at position 7 by chlorine. It is used for the treatment of malaria, hepatic amoebiasis, lupus erythematosus, light-sensitive skin eruptions, and rheumatoid arthritis.
| Excerpt | Relevance | Reference |
|---|---|---|
| "These findings suggest that chloroquine ameliorates atherosclerosis and stabilizes plaque by modulating Tregs differentiation through the regulation of the ATM/AMPK/mTOR pathway." | 8.31 | Chloroquine Alleviates Atherosclerosis by Modulating Regulatory T Cells Through the ATM/AMPK/mTOR Signaling Pathway in ApoE -/- Mice. ( Gao, J; Huang, Q; Li, S; Liu, D; Meng, W; Mo, X; Tian, H; Zhang, Y, 2023) |
| "These findings suggest that chloroquine ameliorates atherosclerosis and stabilizes plaque by modulating Tregs differentiation through the regulation of the ATM/AMPK/mTOR pathway." | 4.31 | Chloroquine Alleviates Atherosclerosis by Modulating Regulatory T Cells Through the ATM/AMPK/mTOR Signaling Pathway in ApoE -/- Mice. ( Gao, J; Huang, Q; Li, S; Liu, D; Meng, W; Mo, X; Tian, H; Zhang, Y, 2023) |
| "Our previous studies have indicated that a novel curcumin derivate nicotinate-curcumin (NC) has beneficial effects on the prevention of atherosclerosis, but the precise mechanisms are not fully understood." | 3.83 | Nicotinate-Curcumin Impedes Foam Cell Formation from THP-1 Cells through Restoring Autophagy Flux. ( Gu, HF; Li, HZ; Liao, DF; Tang, XQ; Tang, YL; Zheng, XL, 2016) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 4 (33.33) | 29.6817 |
| 2010's | 6 (50.00) | 24.3611 |
| 2020's | 2 (16.67) | 2.80 |
| Authors | Studies |
|---|---|
| Rakotondramanana, DL | 1 |
| Delomenède, M | 1 |
| Baltas, M | 1 |
| Duran, H | 1 |
| Bedos-Belval, F | 1 |
| Rasoanaivo, P | 1 |
| Negre-Salvayre, A | 1 |
| Gornitzka, H | 1 |
| Chen, Z | 1 |
| Ouyang, C | 1 |
| Zhang, H | 1 |
| Gu, Y | 1 |
| Deng, Y | 1 |
| Du, C | 1 |
| Cui, C | 1 |
| Li, S | 2 |
| Wang, W | 1 |
| Kong, W | 1 |
| Chen, J | 1 |
| Cai, J | 1 |
| Geng, B | 1 |
| Liu, D | 1 |
| Zhang, Y | 2 |
| Huang, Q | 1 |
| Meng, W | 1 |
| Gao, J | 1 |
| Mo, X | 1 |
| Tian, H | 1 |
| Emanuel, R | 1 |
| Sergin, I | 1 |
| Bhattacharya, S | 1 |
| Turner, J | 1 |
| Epelman, S | 1 |
| Settembre, C | 1 |
| Diwan, A | 1 |
| Ballabio, A | 1 |
| Razani, B | 2 |
| Gu, HF | 1 |
| Li, HZ | 1 |
| Tang, YL | 1 |
| Tang, XQ | 1 |
| Zheng, XL | 1 |
| Liao, DF | 1 |
| Feng, C | 1 |
| Semenkovich, CF | 2 |
| Gu, JQ | 1 |
| Wang, DF | 1 |
| Yan, XG | 1 |
| Zhong, WL | 1 |
| Zhang, J | 1 |
| Fan, B | 1 |
| Ikuyama, S | 1 |
| Ouimet, M | 1 |
| Franklin, V | 1 |
| Mak, E | 1 |
| Liao, X | 1 |
| Tabas, I | 1 |
| Marcel, YL | 1 |
| Karbach, S | 1 |
| Simon, A | 1 |
| Slenzka, A | 1 |
| Jaenecke, I | 1 |
| Habermeier, A | 1 |
| Martiné, U | 1 |
| Förstermann, U | 1 |
| Closs, EI | 1 |
| Shoelson, SE | 1 |
| Schneider, JG | 1 |
| Finck, BN | 1 |
| Ren, J | 1 |
| Standley, KN | 1 |
| Takagi, M | 1 |
| Maclean, KH | 1 |
| Bernal-Mizrachi, C | 1 |
| Muslin, AJ | 1 |
| Kastan, MB | 1 |
| Hamel, P | 1 |
| Abed, E | 1 |
| Brissette, L | 1 |
| Moreau, R | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Metabolic Effects of Hydroxychloroquine[NCT02026232] | 21 participants (Actual) | Interventional | 2012-03-31 | Terminated (stopped due to COVID-19 & loss of funding) | |||
| Genotoxic Stress, Atherosclerosis, and Metabolic Syndrome-AIM 2[NCT00455325] | Phase 2 | 35 participants (Actual) | Interventional | 2004-09-30 | Completed | ||
| Genotoxic Stress, Atherosclerosis, and Metabolic Syndrome- Aim 3[NCT00455403] | 357 participants (Actual) | Interventional | 2006-04-30 | Completed | |||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
determined by fasting blood glucose performed at baseline and follow-up (NCT02026232)
Timeframe: 4 weeks
| Intervention | mg/dL (Mean) | |
|---|---|---|
| Baseline Glucose (mg/dL) | Follow-up Glucose (mg/dL) | |
| Hydroxychloroquine | 186.9 | 165.9 |
| Placebo | 163.1 | 158.8 |
determined by lipid profile with calculated LDL performed at baseline and follow-up (NCT02026232)
Timeframe: 4 weeks
| Intervention | mg/dL (Mean) | |
|---|---|---|
| Baseline - LDL (mg/dL) | Follow-up - LDL (mg/dL) | |
| Hydroxychloroquine | 90.4 | 72.4 |
| Placebo | 92.8 | 87.7 |
Two techniques were employed: auscultation of seated subjects at rest was performed by a trained observer who recorded the first and fifth phases of the Korotkoff sounds; and, a portable oscillometric device (SpaceLabs Medical) recorded results every 20 min during the day and every hour during the night. Data were analyzed as mean values over 24 hours. (NCT00455325)
Timeframe: Assessed every 8-10 weeks at the end of each treatment period.
| Intervention | mmHg (Mean) |
|---|---|
| Placebo Comparator: First Intervention (3 Weeks) | 70 |
| Second Intervention (3 Weeks) | 71 |
| Third Intervention (3 Weeks) | 73 |
| Fourth Intervention (3 Weeks) | 73 |
Hepatic insulin sensitivity was measured by comparing glucose production at baseline of zero insulin infusion rate with glucose production at 56 pmol/m2/min. Hepatic insulin sensitivity was expressed as the percent suppression, such that greater percent suppression indicated greater hepatic insulin sensitivity. There are no reference values, since the patients served as their own controls. (NCT00455325)
Timeframe: assessed every 8 - 10 weeks at the end of each treatment period
| Intervention | % suppression inf rate 56 pmol/m2/min (Mean) |
|---|---|
| Placebo Comparator: First Intervention (3 Weeks) | .56 |
| Second Intervention (3 Weeks) | 0.55 |
| Third Intervention (3 Weeks) | 0.66 |
| Fourth Intervention (3 Weeks) | 0.70 |
Fasting Serum Blood Sample (NCT00455325)
Timeframe: Assessed every 8-10 weeks at the end of each treatment period.
| Intervention | mg/dl (Mean) |
|---|---|
| Placebo Comparator: First Intervention (3 Weeks) | 115 |
| Second Intervention (3 Weeks) | 109 |
| Third Intervention (3 Weeks) | 109 |
| Fourth Intervention (3 Weeks) | 103 |
Fasting Serum Blood Sample (NCT00455325)
Timeframe: Assessed every 8-10 weeks at the end of each treatment period.
| Intervention | mg/dL (Mean) |
|---|---|
| Placebo Comparator: First Intervention (3 Weeks) | 144 |
| Second Intervention (3 Weeks) | 139 |
| Third Intervention (3 Weeks) | 139 |
| Fourth Intervention (3 Weeks) | 131 |
Two techniques were employed: auscultation of seated subjects at rest was performed by a trained observer who recorded the first and fifth phases of the Korotkoff sounds; and, a portable oscillometric device (SpaceLabs Medical) recorded results every 20 min during the day and every hour during the night. Data were analyzed as mean values over 24 hours. (NCT00455325)
Timeframe: Assessed every 8-10 weeks at the end of each treatment period
| Intervention | mmHg (Mean) |
|---|---|
| Placebo Comparator: First Intervention (3 Weeks) | 121 |
| Second Intervention (3 Weeks) | 121 |
| Third Intervention (3 Weeks) | 123 |
| Fourth Intervention (3 Weeks) | 123 |
Fasting Serum Blood Sample (NCT00455325)
Timeframe: Assessed every 8-10 weeks at the end of each treatment period.
| Intervention | mg/dL (Mean) |
|---|---|
| Placebo Comparator: First Intervention (3 Weeks) | 187 |
| Second Intervention (3 Weeks) | 181 |
| Third Intervention (3 Weeks) | 182 |
| Fourth Intervention (3 Weeks) | 173 |
Fasting Serum Blood Sample (NCT00455325)
Timeframe: Assessed every 8-10 weeks at the end of each treatment period.
| Intervention | mg/dL (Mean) |
|---|---|
| Placebo Comparator: First Intervention (3 Weeks) | 143 |
| Second Intervention (3 Weeks) | 153 |
| Third Intervention (3 Weeks) | 151 |
| Fourth Intervention (3 Weeks) | 140 |
A noninvasive predictor of cardiovascular events, Carotid artery intima-media thickness (CIMT) was measured from B-mode images by a single sonographer using standard approaches (NCT00455403)
Timeframe: Measured at baseline and year 1
| Intervention | millmeter (Mean) | |
|---|---|---|
| Baseline | Year 1 | |
| Chloroquine Subjects | 0.766 | 0.758 |
| Placebo Subjects | 0.765 | 0.768 |
1 review available for chloroquine and Atherogenesis
| Article | Year |
|---|---|
Banking on ATM as a new target in metabolic syndrome.
Topics: Animals; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Cell Cycle Proteins; Chloroquine; | 2006 |
11 other studies available for chloroquine and Atherogenesis
| Article | Year |
|---|---|
Synthesis of ferulic ester dimers, functionalisation and biological evaluation as potential antiatherogenic and antiplasmodial agents.
Topics: Animals; Antioxidants; Atherosclerosis; Cell Survival; Coumaric Acids; Dimerization; Endothelium, Va | 2007 |
Vascular smooth muscle cell-derived hydrogen sulfide promotes atherosclerotic plaque stability via TFEB (transcription factor EB)-mediated autophagy.
Topics: Atherosclerosis; Autophagy; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; Biomarkers; | 2022 |
Chloroquine Alleviates Atherosclerosis by Modulating Regulatory T Cells Through the ATM/AMPK/mTOR Signaling Pathway in ApoE -/- Mice.
Topics: AMP-Activated Protein Kinases; Animals; Apolipoproteins E; Ataxia Telangiectasia; Atherosclerosis; C | 2023 |
Induction of lysosomal biogenesis in atherosclerotic macrophages can rescue lipid-induced lysosomal dysfunction and downstream sequelae.
Topics: Animals; Apolipoproteins E; Atherosclerosis; Autophagy; Autophagy-Related Protein 5; Basic Helix-Loo | 2014 |
Nicotinate-Curcumin Impedes Foam Cell Formation from THP-1 Cells through Restoring Autophagy Flux.
Topics: Adenine; Atherosclerosis; Autophagy; Cell Line; Chloroquine; Cholesterol; Curcumin; Foam Cells; Huma | 2016 |
p53 is required for chloroquine-induced atheroprotection but not insulin sensitization.
Topics: Animals; Antimalarials; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Blood Glucose; Cell | 2010 |
p53 is required for chloroquine-induced atheroprotection but not insulin sensitization.
Topics: Animals; Antimalarials; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Blood Glucose; Cell | 2010 |
p53 is required for chloroquine-induced atheroprotection but not insulin sensitization.
Topics: Animals; Antimalarials; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Blood Glucose; Cell | 2010 |
p53 is required for chloroquine-induced atheroprotection but not insulin sensitization.
Topics: Animals; Antimalarials; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Blood Glucose; Cell | 2010 |
p53 is required for chloroquine-induced atheroprotection but not insulin sensitization.
Topics: Animals; Antimalarials; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Blood Glucose; Cell | 2010 |
p53 is required for chloroquine-induced atheroprotection but not insulin sensitization.
Topics: Animals; Antimalarials; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Blood Glucose; Cell | 2010 |
p53 is required for chloroquine-induced atheroprotection but not insulin sensitization.
Topics: Animals; Antimalarials; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Blood Glucose; Cell | 2010 |
p53 is required for chloroquine-induced atheroprotection but not insulin sensitization.
Topics: Animals; Antimalarials; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Blood Glucose; Cell | 2010 |
p53 is required for chloroquine-induced atheroprotection but not insulin sensitization.
Topics: Animals; Antimalarials; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Blood Glucose; Cell | 2010 |
A Toll-like receptor 9-mediated pathway stimulates perilipin 3 (TIP47) expression and induces lipid accumulation in macrophages.
Topics: Animals; Atherosclerosis; Blotting, Western; Carrier Proteins; Cell Line; Chloroquine; Female; JNK M | 2010 |
Autophagy regulates cholesterol efflux from macrophage foam cells via lysosomal acid lipase.
Topics: Animals; Atherosclerosis; Autophagy; Autophagy-Related Protein 5; Bone Marrow Cells; Cells, Cultured | 2011 |
Relative contribution of different l-arginine sources to the substrate supply of endothelial nitric oxide synthase.
Topics: Arginine; Atherosclerosis; Biological Transport; Cell Line; Chloroquine; Chromatography, High Pressu | 2011 |
ATM-dependent suppression of stress signaling reduces vascular disease in metabolic syndrome.
Topics: Animals; Apolipoproteins E; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Cell Cycle Prot | 2006 |
ATM-dependent suppression of stress signaling reduces vascular disease in metabolic syndrome.
Topics: Animals; Apolipoproteins E; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Cell Cycle Prot | 2006 |
ATM-dependent suppression of stress signaling reduces vascular disease in metabolic syndrome.
Topics: Animals; Apolipoproteins E; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Cell Cycle Prot | 2006 |
ATM-dependent suppression of stress signaling reduces vascular disease in metabolic syndrome.
Topics: Animals; Apolipoproteins E; Ataxia Telangiectasia Mutated Proteins; Atherosclerosis; Cell Cycle Prot | 2006 |
Characterization of oxidized low-density lipoprotein-induced hormesis-like effects in osteoblastic cells.
Topics: Animals; Apoptosis; Atherosclerosis; Cell Line; Cell Proliferation; Chloroquine; Humans; Lipoprotein | 2008 |