hydrochlorothiazide has been researched along with Fibrosis in 9 studies
Hydrochlorothiazide: A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.
hydrochlorothiazide : A benzothiadiazine that is 3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide substituted by a chloro group at position 6 and a sulfonamide at 7. It is diuretic used for the treatment of hypertension and congestive heart failure.
Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.
| Excerpt | Relevance | Reference |
|---|---|---|
| "In patients with hypertensive heart disease, angiotensin-converting enzyme inhibition with lisinopril can regress myocardial fibrosis, irrespective of LVH regression, and it is accompanied by improved LV diastolic function." | 9.09 | Lisinopril-mediated regression of myocardial fibrosis in patients with hypertensive heart disease. ( Brilla, CG; Funck, RC; Rupp, H, 2000) |
| "Thiazides are one of the most common antihypertensive drugs used for hypertension treatment and hydrochlorothiazide (HCTZ) is the most frequently used diuretic for hypertension treatment." | 8.02 | Hydrochlorothiazide Reduces Cardiac Hypertrophy, Fibrosis and Rho-Kinase Activation in DOCA-Salt Induced Hypertension. ( Araos, P; Jalil, JE; Mondaca-Ruff, D; Mora, IG; Novoa, UF; Ocaranza, MP; Yañez, CE, 2021) |
| "Our previous study indicates that hydrochlorothiazide inhibits transforming growth factor (TGF)-β/Smad signaling pathway, improves cardiac function and reduces fibrosis." | 7.85 | Hydrochlorothiazide modulates ischemic heart failure-induced cardiac remodeling via inhibiting angiotensin II type 1 receptor pathway in rats. ( Chen, X; Gao, X; Lu, G; Luo, C; Luo, J; Peng, L; Zuo, Z, 2017) |
| "In patients with hypertensive heart disease, angiotensin-converting enzyme inhibition with lisinopril can regress myocardial fibrosis, irrespective of LVH regression, and it is accompanied by improved LV diastolic function." | 5.09 | Lisinopril-mediated regression of myocardial fibrosis in patients with hypertensive heart disease. ( Brilla, CG; Funck, RC; Rupp, H, 2000) |
| "Thiazides are one of the most common antihypertensive drugs used for hypertension treatment and hydrochlorothiazide (HCTZ) is the most frequently used diuretic for hypertension treatment." | 4.02 | Hydrochlorothiazide Reduces Cardiac Hypertrophy, Fibrosis and Rho-Kinase Activation in DOCA-Salt Induced Hypertension. ( Araos, P; Jalil, JE; Mondaca-Ruff, D; Mora, IG; Novoa, UF; Ocaranza, MP; Yañez, CE, 2021) |
| "Our previous study indicates that hydrochlorothiazide inhibits transforming growth factor (TGF)-β/Smad signaling pathway, improves cardiac function and reduces fibrosis." | 3.85 | Hydrochlorothiazide modulates ischemic heart failure-induced cardiac remodeling via inhibiting angiotensin II type 1 receptor pathway in rats. ( Chen, X; Gao, X; Lu, G; Luo, C; Luo, J; Peng, L; Zuo, Z, 2017) |
| " 1D11, diltiazem, and hydrochlorothiazide (HCT) attenuated the development of hypertension, proteinuria, and glomerular injury." | 3.78 | Renoprotective effects of anti-TGF-β antibody and antihypertensive therapies in Dahl S rats. ( Chen, CC; Dahly-Vernon, AJ; Dunn, KM; Ledbetter, SR; Murphy, SR; Roman, RJ; Williams, JM, 2012) |
| "The aim was to compare the effects of two diuretics, indapamide and hydrochlorothiazide, on cardiac hypertrophy in stroke prone spontaneously hypertensive rats (SHR-SP)." | 3.68 | Diuretic effects on cardiac hypertrophy in the stroke prone spontaneously hypertensive rat. ( Contard, F; Glukhova, M; Guez, D; Marotte, F; Narcisse, G; Rappaport, L; Samuel, JL; Schatz, C; Swynghedauw, B, 1993) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 1 (11.11) | 18.2507 |
| 2000's | 3 (33.33) | 29.6817 |
| 2010's | 4 (44.44) | 24.3611 |
| 2020's | 1 (11.11) | 2.80 |
| Authors | Studies |
|---|---|
| Mondaca-Ruff, D | 1 |
| Araos, P | 1 |
| Yañez, CE | 1 |
| Novoa, UF | 1 |
| Mora, IG | 1 |
| Ocaranza, MP | 1 |
| Jalil, JE | 1 |
| Wei, SY | 1 |
| Wang, YX | 1 |
| Zhang, QF | 1 |
| Zhao, SL | 1 |
| Diao, TT | 1 |
| Li, JS | 1 |
| Qi, WR | 1 |
| He, YX | 1 |
| Guo, XY | 1 |
| Zhang, MZ | 1 |
| Chen, JY | 1 |
| Wang, XT | 1 |
| Wei, QJ | 1 |
| Wang, Y | 1 |
| Li, B | 1 |
| Luo, J | 1 |
| Chen, X | 1 |
| Luo, C | 1 |
| Lu, G | 1 |
| Peng, L | 1 |
| Gao, X | 1 |
| Zuo, Z | 1 |
| Murphy, SR | 1 |
| Dahly-Vernon, AJ | 1 |
| Dunn, KM | 1 |
| Chen, CC | 1 |
| Ledbetter, SR | 1 |
| Williams, JM | 1 |
| Roman, RJ | 1 |
| Villa, L | 1 |
| Boor, P | 1 |
| Konieczny, A | 1 |
| Kunter, U | 1 |
| van Roeyen, CR | 1 |
| Denecke, B | 1 |
| Gan, L | 1 |
| Neusser, MA | 1 |
| Cohen, CD | 1 |
| Eitner, F | 1 |
| Scholl, T | 1 |
| Ostendorf, T | 1 |
| Floege, J | 1 |
| Gröholm, T | 1 |
| Finckenberg, P | 1 |
| Palojoki, E | 1 |
| Saraste, A | 1 |
| Bäcklund, T | 1 |
| Eriksson, A | 1 |
| Laine, M | 1 |
| Mervaala, E | 1 |
| Tikkanen, I | 1 |
| Contard, F | 1 |
| Glukhova, M | 1 |
| Marotte, F | 1 |
| Narcisse, G | 1 |
| Schatz, C | 1 |
| Swynghedauw, B | 1 |
| Guez, D | 1 |
| Samuel, JL | 1 |
| Rappaport, L | 1 |
| Brilla, CG | 2 |
| Funck, RC | 1 |
| Rupp, H | 1 |
1 trial available for hydrochlorothiazide and Fibrosis
| Article | Year |
|---|---|
Lisinopril-mediated regression of myocardial fibrosis in patients with hypertensive heart disease.
Topics: Adolescent; Adult; Aged; Analysis of Variance; Angiotensin-Converting Enzyme Inhibitors; Antihyperte | 2000 |
8 other studies available for hydrochlorothiazide and Fibrosis
| Article | Year |
|---|---|
Hydrochlorothiazide Reduces Cardiac Hypertrophy, Fibrosis and Rho-Kinase Activation in DOCA-Salt Induced Hypertension.
Topics: Animals; Antihypertensive Agents; Blood Pressure; Cardiomegaly; Connective Tissue Growth Factor; Fib | 2021 |
Multiple Mechanisms are Involved in Salt-Sensitive Hypertension-Induced Renal Injury and Interstitial Fibrosis.
Topics: Animals; Antihypertensive Agents; Blood Pressure; Capillaries; Fibrosis; Hydrochlorothiazide; Hypert | 2017 |
Hydrochlorothiazide modulates ischemic heart failure-induced cardiac remodeling via inhibiting angiotensin II type 1 receptor pathway in rats.
Topics: Aldosterone; Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Animals, Newborn; Cel | 2017 |
Renoprotective effects of anti-TGF-β antibody and antihypertensive therapies in Dahl S rats.
Topics: Acute Kidney Injury; Animals; Antibodies, Anti-Idiotypic; Antihypertensive Agents; Blood Pressure; C | 2012 |
Late angiotensin II receptor blockade in progressive rat mesangioproliferative glomerulonephritis: new insights into mechanisms.
Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Antihypertensive Agents; Atenolol; Benzimidazoles; | 2013 |
Cardioprotective effects of vasopeptidase inhibition vs. angiotensin type 1-receptor blockade in spontaneously hypertensive rats on a high salt diet.
Topics: Aldosterone; Angiotensin II Type 1 Receptor Blockers; Animals; Antihypertensive Agents; Apoptosis; A | 2004 |
Diuretic effects on cardiac hypertrophy in the stroke prone spontaneously hypertensive rat.
Topics: Animals; Blood Pressure; Cardiomegaly; Coronary Vessels; Drug Evaluation, Preclinical; Fibrosis; Hyd | 1993 |
Renin-angiotensin system mediated mechanisms: cardioreparation and cardioprotection.
Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Diuretics; Female; Fibrosis; Heart Failure; Human | 2000 |