metformin has been researched along with Pulmonary Hypertension in 17 studies
Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289)
metformin : A member of the class of guanidines that is biguanide the carrying two methyl substituents at position 1.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Our data suggest a potential use of treprostinil as an early treatment for mild metabolic syndrome-associated PH-HFpEF and that combined treatment with treprostinil and metformin may improve hyperglycemia and cardiac function in a more severe disease." | 7.96 | Treatment With Treprostinil and Metformin Normalizes Hyperglycemia and Improves Cardiac Function in Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction. ( Avolio, T; Bachman, TN; Bai, Y; Baust, JJ; Bonetto, A; Considine, RV; Cook, T; Fisher, A; Gladwin, MT; Goncharov, DA; Goncharova, EA; Halliday, G; Hu, J; Huot, JR; Lai, YC; Machado, RF; McTiernan, CF; Mora, AL; Satoh, T; Sebastiani, A; Tan, J; Vanderpool, RR; Wang, L, 2020) |
| "Chronic oral nitrite treatment improved hyperglycemia in obese ZSF1 rats by a process that requires skeletal muscle SIRT3-AMPK-GLUT4 signaling." | 5.43 | SIRT3-AMP-Activated Protein Kinase Activation by Nitrite and Metformin Improves Hyperglycemia and Normalizes Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction. ( Dube, JJ; Garcia-Ocaña, A; Gladwin, MT; Goncharov, DA; Goncharova, EA; Hughan, KS; Lai, YC; Mora, AL; St Croix, CM; Tabima, DM; Tofovic, SP; Vanderpool, RR, 2016) |
| "Metformin effects were analysed in hypoxia- and monocrotaline-induced PAH in rats." | 5.35 | Protective role of the antidiabetic drug metformin against chronic experimental pulmonary hypertension. ( Agard, C; Dumas-de-La-Roque, E; Loirand, G; Pacaud, P; Rio, M; Rolli-Derkinderen, M; Sagan, C; Savineau, JP, 2009) |
| "Our data suggest a potential use of treprostinil as an early treatment for mild metabolic syndrome-associated PH-HFpEF and that combined treatment with treprostinil and metformin may improve hyperglycemia and cardiac function in a more severe disease." | 3.96 | Treatment With Treprostinil and Metformin Normalizes Hyperglycemia and Improves Cardiac Function in Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction. ( Avolio, T; Bachman, TN; Bai, Y; Baust, JJ; Bonetto, A; Considine, RV; Cook, T; Fisher, A; Gladwin, MT; Goncharov, DA; Goncharova, EA; Halliday, G; Hu, J; Huot, JR; Lai, YC; Machado, RF; McTiernan, CF; Mora, AL; Satoh, T; Sebastiani, A; Tan, J; Vanderpool, RR; Wang, L, 2020) |
| "Metformin is an activator of the AMPK and Nrf2 pathways which are important in the pathology of several complex pulmonary diseases with unmet medical needs." | 1.56 | Inhalable Nanoparticles/Microparticles of an AMPK and Nrf2 Activator for Targeted Pulmonary Drug Delivery as Dry Powder Inhalers. ( Abrahamson, MD; Acosta, MF; Black, SM; Encinas-Basurto, D; Fineman, JR; Mansour, HM, 2020) |
| "Chronic oral nitrite treatment improved hyperglycemia in obese ZSF1 rats by a process that requires skeletal muscle SIRT3-AMPK-GLUT4 signaling." | 1.43 | SIRT3-AMP-Activated Protein Kinase Activation by Nitrite and Metformin Improves Hyperglycemia and Normalizes Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction. ( Dube, JJ; Garcia-Ocaña, A; Gladwin, MT; Goncharov, DA; Goncharova, EA; Hughan, KS; Lai, YC; Mora, AL; St Croix, CM; Tabima, DM; Tofovic, SP; Vanderpool, RR, 2016) |
| "Metformin (MET) was administered to activate AMPK." | 1.43 | Activation of AMPK Prevents Monocrotaline-Induced Extracellular Matrix Remodeling of Pulmonary Artery. ( Han, D; Ke, R; Li, M; Li, S; Liu, L; Song, Y; Xie, X; Yang, L; Zhang, Y; Zhu, Y, 2016) |
| " In conclusion, activation of AMPK restores angiogenesis and increases the bioavailability of nitric oxide in IPH." | 1.39 | AMP kinase activation improves angiogenesis in pulmonary artery endothelial cells with in utero pulmonary hypertension. ( Afolayan, AJ; Du, J; Eis, A; Konduri, GG; Shi, Y; Teng, RJ, 2013) |
| "Metformin effects were analysed in hypoxia- and monocrotaline-induced PAH in rats." | 1.35 | Protective role of the antidiabetic drug metformin against chronic experimental pulmonary hypertension. ( Agard, C; Dumas-de-La-Roque, E; Loirand, G; Pacaud, P; Rio, M; Rolli-Derkinderen, M; Sagan, C; Savineau, JP, 2009) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 1 (5.88) | 29.6817 |
| 2010's | 10 (58.82) | 24.3611 |
| 2020's | 6 (35.29) | 2.80 |
| Authors | Studies |
|---|---|
| McNair, BD | 1 |
| Polson, SM | 1 |
| Shorthill, SK | 1 |
| Yusifov, A | 1 |
| Walker, LA | 1 |
| Weiser-Evans, MCM | 1 |
| Kovacs, EJ | 1 |
| Bruns, DR | 1 |
| Rana, U | 1 |
| Callan, E | 1 |
| Entringer, B | 1 |
| Michalkiewicz, T | 1 |
| Joshi, A | 1 |
| Parchur, AK | 1 |
| Teng, RJ | 2 |
| Konduri, GG | 2 |
| Wang, L | 1 |
| Halliday, G | 1 |
| Huot, JR | 1 |
| Satoh, T | 1 |
| Baust, JJ | 2 |
| Fisher, A | 1 |
| Cook, T | 1 |
| Hu, J | 2 |
| Avolio, T | 1 |
| Goncharov, DA | 3 |
| Bai, Y | 1 |
| Vanderpool, RR | 3 |
| Considine, RV | 1 |
| Bonetto, A | 1 |
| Tan, J | 1 |
| Bachman, TN | 1 |
| Sebastiani, A | 1 |
| McTiernan, CF | 1 |
| Mora, AL | 3 |
| Machado, RF | 1 |
| Goncharova, EA | 3 |
| Gladwin, MT | 4 |
| Lai, YC | 4 |
| Wang, D | 1 |
| Mao, Y | 1 |
| Wang, T | 1 |
| Xiong, T | 1 |
| Yang, X | 1 |
| Komamura, K | 1 |
| Acosta, MF | 1 |
| Abrahamson, MD | 1 |
| Encinas-Basurto, D | 1 |
| Fineman, JR | 1 |
| Black, SM | 1 |
| Mansour, HM | 1 |
| Tofovic, SP | 2 |
| Pena, AZ | 1 |
| Ray, A | 1 |
| Rode, A | 1 |
| Sun, Z | 1 |
| Liu, Y | 1 |
| Yu, F | 1 |
| Xu, Y | 1 |
| Yanli, L | 1 |
| Liu, N | 1 |
| Xiaolu, W | 1 |
| Yunliang, G | 1 |
| Tabima, DM | 1 |
| Dube, JJ | 1 |
| Hughan, KS | 1 |
| St Croix, CM | 1 |
| Garcia-Ocaña, A | 1 |
| Li, S | 1 |
| Han, D | 1 |
| Zhang, Y | 1 |
| Xie, X | 1 |
| Ke, R | 1 |
| Zhu, Y | 1 |
| Liu, L | 1 |
| Song, Y | 1 |
| Yang, L | 1 |
| Li, M | 1 |
| Houssaini, A | 1 |
| Abid, S | 1 |
| Derumeaux, G | 1 |
| Wan, F | 1 |
| Parpaleix, A | 1 |
| Rideau, D | 1 |
| Marcos, E | 1 |
| Kebe, K | 1 |
| Czibik, G | 1 |
| Sawaki, D | 1 |
| Treins, C | 1 |
| Dubois-Randé, JL | 1 |
| Li, Z | 1 |
| Amsellem, V | 1 |
| Lipskaia, L | 1 |
| Pende, M | 1 |
| Adnot, S | 1 |
| Dean, A | 1 |
| Nilsen, M | 1 |
| Loughlin, L | 1 |
| Salt, IP | 1 |
| MacLean, MR | 1 |
| Carlström, M | 1 |
| Lundberg, JO | 1 |
| Agard, C | 1 |
| Rolli-Derkinderen, M | 1 |
| Dumas-de-La-Roque, E | 1 |
| Rio, M | 1 |
| Sagan, C | 1 |
| Savineau, JP | 1 |
| Loirand, G | 1 |
| Pacaud, P | 1 |
| Du, J | 1 |
| Afolayan, AJ | 1 |
| Eis, A | 1 |
| Shi, Y | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Dose Escalation Study to Evaluate the Effect of Inhaled Nitrite on Cardiopulmonary Hemodynamics in Subjects With Pulmonary Hypertension[NCT01431313] | Phase 2 | 48 participants (Actual) | Interventional | 2012-06-30 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Basal platelet oxygen consumption measured in isolated platelets by extracellular flux analysis (XF24, Seahorse Biosciences, Billerica, MA). (NCT01431313)
Timeframe: Maximal effect at 15 minutes post 45mg or 90mg inhalation vs Pre dose
| Intervention | picomoles O2/min (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | -17.58 |
| WHO Group II Pulmonary Hypertension (PH) | 8.62 |
| WHO Group III Pulmonary Hypertension (PH) | -11.64 |
Linear mixed effects model across all time points and doses relative to baseline. The mixed effects model takes into account all time points combined (repeated measures) and has been extensively described for clinical trials (please see references). In this model, the effect of treatment on hemodynamics (measured at 0, 15, 30, 45, and 60 minutes after 45mg followed by same times after 90 mg dose) was compared with baseline values. We assessed the overall linear trend of treatment. The effect of treatment on hemodynamics in each patient group was assessed separately in mixed-effects models. The reported mean is the change from baseline of plasma nitrite concentrations in mixed venous blood over all subsequent times and doses (beta from the mixed effects model), and is reported as the mean and 95% confidence interval. (NCT01431313)
Timeframe: Pre-dose, 15 minutes post 45mg and 90mg inhalation
| Intervention | micromolar (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | 9.9 |
| WHO Group II Pulmonary Hypertension (PH) | 7.0 |
| WHO Group III Pulmonary Hypertension (PH) | 7.4 |
Linear mixed effects model across all time points and doses relative to baseline. The mixed effects model takes into account all time points combined (repeated measures) and has been extensively described for clinical trials (please see references). In this model, the effect of treatment on hemodynamics (measured at 0, 15, 30, 45, and 60 minutes after 45mg followed by same times after 90 mg dose) was compared with baseline values. We assessed the overall linear trend of treatment. The effect of treatment on hemodynamics in each patient group was assessed separately in mixed-effects models. The reported mean is the change from baseline of pulmonary artery occlusion (capillary) pullback nitrite concentration over all subsequent times and doses (beta from the mixed effects model), and is reported as the mean and 95% confidence interval. (NCT01431313)
Timeframe: Pre-dose, 15 minutes post 45mg and 90mg inhalation
| Intervention | micromolar (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | 9.2 |
| WHO Group III Pulmonary Hypertension (PH) | 2.4 |
Characteristic impedance (Zc) which may be related to compliance effects in the large, conduit arteries. (NCT01431313)
Timeframe: Pre dose and 60 minutes post last dosage inhaled
| Intervention | dyne*sec/cm5 (Median) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | -0.004 |
| WHO Group II Pulmonary Hypertension (PH) | -0.34 |
| WHO Group III Pulmonary Hypertension (PH) | -0.20 |
Linear mixed effects model across all time points and doses relative to baseline. The mixed effects model takes into account all time points combined (repeated measures) and has been extensively described for clinical trials (please see references). In this model, the effect of treatment on hemodynamics (measured at 0, 15, 30, 45, and 60 minutes after 45mg followed by same times after 90 mg dose) was compared with baseline values. We assessed the overall linear trend of treatment. The effect of treatment on hemodynamics in each patient group was assessed separately in mixed-effects models. Since pulmonary vascular resistance (PVR) was not normally distributed, it was transformed to natural log prior to analysis. The reported mean is the change from baseline of PVR over all subsequent times and doses (beta from the mixed effects model, converted back from natural log to Woods units), and is reported as the mean and 95% confidence interval. (NCT01431313)
Timeframe: Time zero, 15, 30, 45 and 60 minutes after nebulization of 45mg followed by 90 mg dose
| Intervention | Woods units (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | 0.77 |
| WHO Group II Pulmonary Hypertension (PH) | 0.40 |
| WHO Group III Pulmonary Hypertension (PH) | -0.39 |
Linear mixed effects model across all time points and doses relative to baseline. The mixed effects model takes into account all time points combined (repeated measures) and has been extensively described for clinical trials (please see references). In this model, the effect of treatment on hemodynamics (measured at 0, 15, 30, 45, and 60 minutes after 45mg followed by same times after 90 mg dose) was compared with baseline values. We assessed the overall linear trend of treatment. The effect of treatment on hemodynamics in each patient group was assessed separately in mixed-effects models. The reported mean is the change from baseline of MAP over all subsequent times and doses (beta from the mixed effects model), and is reported as the mean and 95% confidence interval. (NCT01431313)
Timeframe: Time zero, 15, 30, 45 and 60 minutes after nebulization of 45mg followed by 90 mg dose
| Intervention | mmHg (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | -5.1 |
| WHO Group II Pulmonary Hypertension (PH) | -3.4 |
| WHO Group III Pulmonary Hypertension (PH) | -9.5 |
Linear mixed effects model across all time points and doses relative to baseline. The mixed effects model takes into account all time points combined (repeated measures) and has been extensively described for clinical trials (please see references). In this model, the effect of treatment on hemodynamics (measured at 0, 15, 30, 45, and 60 minutes after 45mg followed by same times after 90 mg dose) was compared with baseline values. We assessed the overall linear trend of treatment. The effect of treatment on hemodynamics in each patient group was assessed separately in mixed-effects models. Since systemic vascular resistance was not normally distributed, it was transformed to natural log prior to analysis. The reported mean is the change from baseline of SVR over all subsequent times and doses (beta from the mixed effects model), and is reported as the mean and 95% confidence interval. (NCT01431313)
Timeframe: Time zero, 15, 30, 45 and 60 minutes after nebulization of 45mg followed by 90 mg dose
| Intervention | mmHg⋅min/L (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | -0.43 |
| WHO Group II Pulmonary Hypertension (PH) | 1.19 |
| WHO Group III Pulmonary Hypertension (PH) | -2.04 |
Time in minutes to maximum PVR decrease. During study procedure, hemodynamics were measured at 0, 15, 30, 45, and 60 minutes after 45 mg followed by same times after 90 mg dose. The time point at which each patient's maximal decrease in PVR occurred was recorded and reported as the mean and standard deviation in each cohort. (NCT01431313)
Timeframe: 0, 15, 30, 45, and 60 minutes after 45 mg followed by same times after 90 mg dose
| Intervention | minutes (Mean) |
|---|---|
| WHO Group I Pulmonary Arterial Hypertension (PAH) | 42.0 |
| WHO Group II Pulmonary Hypertension (PH) | 33.0 |
| WHO Group III Pulmonary Hypertension (PH) | 42.5 |
17 other studies available for metformin and Pulmonary Hypertension
| Article | Year |
|---|---|
Metformin protects against pulmonary hypertension-induced right ventricular dysfunction in an age- and sex-specific manner independent of cardiac AMPK.
Topics: AMP-Activated Protein Kinases; Animals; Disease Models, Animal; Female; Heart Failure; Hypertension, | 2023 |
AMP-Kinase Dysfunction Alters Notch Ligands to Impair Angiogenesis in Neonatal Pulmonary Hypertension.
Topics: AMP-Activated Protein Kinase Kinases; Animals; Animals, Newborn; Biphenyl Compounds; Ductus Arterios | 2020 |
Treatment With Treprostinil and Metformin Normalizes Hyperglycemia and Improves Cardiac Function in Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction.
Topics: AMP-Activated Protein Kinases; Animals; Antihypertensive Agents; Diet, High-Fat; Epoprostenol; Heart | 2020 |
Letter by Wang et al Regarding Article, "Treatment With Treprostinil and Metformin Normalizes Hyperglycemia and Improves Cardiac Function in Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction".
Topics: Epoprostenol; Heart Failure; Humans; Hyperglycemia; Hypertension, Pulmonary; Metformin; Stroke Volum | 2020 |
Letter by Komamura Regarding Article, "Treatment With Treprostinil and Metformin Normalizes Hyperglycemia and Improves Cardiac Function in Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction".
Topics: Epoprostenol; Heart Failure; Humans; Hyperglycemia; Hypertension, Pulmonary; Metformin; Stroke Volum | 2020 |
Inhalable Nanoparticles/Microparticles of an AMPK and Nrf2 Activator for Targeted Pulmonary Drug Delivery as Dry Powder Inhalers.
Topics: Administration, Inhalation; Aerosols; AMP-Activated Protein Kinases; Cell Line; Drug Compounding; Dr | 2020 |
Metformin Therapy for Pulmonary Hypertension Associated with Heart Failure with Preserved Ejection Fraction versus Pulmonary Arterial Hypertension.
Topics: Animals; Disease Models, Animal; Familial Primary Pulmonary Hypertension; Heart Failure; Hypertensio | 2018 |
Long non-coding RNA and mRNA profile analysis of metformin to reverse the pulmonary hypertension vascular remodeling induced by monocrotaline.
Topics: Animals; Cell Cycle; Cell Proliferation; Cells, Cultured; Gene Expression Regulation; Gene Ontology; | 2019 |
Letter by Wang and Guo regarding article Long non-coding RNA and mRNA profile analysis of metformin to reverse the pulmonary hypertension vascular remodeling induced by monocrotaline.
Topics: Humans; Hypertension, Pulmonary; Metformin; Monocrotaline; Pulmonary Artery; RNA, Long Noncoding; RN | 2019 |
SIRT3-AMP-Activated Protein Kinase Activation by Nitrite and Metformin Improves Hyperglycemia and Normalizes Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction.
Topics: AMP-Activated Protein Kinases; Animals; Cells, Cultured; Enzyme Activation; Heart Failure; Humans; H | 2016 |
Activation of AMPK Prevents Monocrotaline-Induced Extracellular Matrix Remodeling of Pulmonary Artery.
Topics: AMP-Activated Protein Kinases; Animals; Disease Models, Animal; Enzyme Activation; Extracellular Mat | 2016 |
Selective Tuberous Sclerosis Complex 1 Gene Deletion in Smooth Muscle Activates Mammalian Target of Rapamycin Signaling and Induces Pulmonary Hypertension.
Topics: Animals; Cell Proliferation; Cells, Cultured; Chronic Disease; Gene Deletion; Hyperplasia; Hypertens | 2016 |
Metformin Reverses Development of Pulmonary Hypertension via Aromatase Inhibition.
Topics: AMP-Activated Protein Kinases; Animals; Aromatase; Aromatase Inhibitors; Cell Line; Cell Proliferati | 2016 |
Letter by Carlström and Lundberg Regarding Article, "SIRT3-AMP-Activated Protein Kinase Activation by Nitrite and Metformin Improves Hyperglycemia and Normalizes Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction".
Topics: AMP-Activated Protein Kinases; Heart Failure; Humans; Hyperglycemia; Hypertension, Pulmonary; Metfor | 2016 |
Response by Lai and Gladwin to Letter Regarding Article, "SIRT3-AMP-Activated Protein Kinase Activation by Nitrite and Metformin Improves Hyperglycemia and Normalizes Pulmonary Hypertension Associated With Heart Failure With Preserved Ejection Fraction".
Topics: AMP-Activated Protein Kinases; Heart Failure; Humans; Hyperglycemia; Hypertension, Pulmonary; Metfor | 2016 |
Protective role of the antidiabetic drug metformin against chronic experimental pulmonary hypertension.
Topics: Animals; Cell Proliferation; Chronic Disease; Endothelium, Vascular; Enzyme Activation; Hemodynamics | 2009 |
AMP kinase activation improves angiogenesis in pulmonary artery endothelial cells with in utero pulmonary hypertension.
Topics: AMP-Activated Protein Kinases; Animals; Caveolin 1; Cells, Cultured; Endothelial Cells; Enzyme Activ | 2013 |