Sprague-Dawley rats and cardiomyocytes |
20 μM, 2 h |
Short-term treatment with Ang II attenuates the transversal YM in isolated adult rat cardiomyocytes acting via an AT1 R |
High sample indentation in direct contact mode or lack of selectivity or that makes it difficult to assess the sample–probe interaction |
Swiatlowska et al. (2020)
|
Long exposure time to high-intensity light affecting cell enzymatic reactions, difficulty in manufacturing instruments, time-consuming measurements |
C57BL/6J mice & Primary cardiomyocytes from C57BL/6J mice |
2.5 mg/kg/day, s.c., 2 weeks. 100 nM, 24 h |
Administration of Ang II increases the expression of miR-154-5p and cardiac remodeling concurrently. miR-154-5p interacts with 3′ UTR and inhibits arylsulfatase B to trigger cardiomyocyte apoptosis and hypertrophy associated with oxidative stress |
The hypothesis of miR-154-5p promoting hypertrophy needs further testing in the near future |
Wang Q. et al. (2019)
|
|
HEK293T, HEK293-AT1R, and HEK293T-SIN1−/− cells |
200 nM |
SGK1 activation occurs at a distinct subcellular compartment from that of Akt |
The use of SIN1 and SGK1 overexpression since overexpression of these proteins might influence their subcellular localization. |
Gleason et al. (2019)
|
ApoE−/− mice |
750 µg/kg/day, s. c. |
Ang II increases the expression of EMMPRIN in atherosclerotic plaque |
Further research is required to elucidate details of the mechanism involved |
Zhang Y. et al. (2019)
|
Amniotic fluid mesenchymal stem cells |
0.1 and 1 μM |
Ang II and TGF-β1 are efficient cardiomyogenic inducers of human AF-MSCs; They initiate protein expression, alterations at the gene and epigenetic levels in stem cells leading towards cardiomyocyte-like phenotype formation. |
|
Gasiūnienė et al. (2019)
|
Male silent information regulator 1 (SIRT1) flox/flox and cardiomyocyte-specific inducible SIRT1 knockout mice (SIRT1-iKO) |
1.1 mg/kg/day for 4 weeks |
FGF21 improves cardiac function and alleviates Ang II-induced cardiac hypertrophy in a SIRT1-dependent manner |
Presence of a small number of animals in a group |
Li et al. (2019)
|
CRFK cells (feline kidney epithelial cell line) |
- |
Ang II shows a similar result to TGF-β1 if the AT1 R was expressed more in CRFK cells |
The experiment could have involved other cells. |
van Beusekom and Zimmering, (2019)
|
C57BL/6J mice |
1.5 μg/min/kg, s.c., 4 weeks |
Soluble receptors for advanced glycation end-products were evidenced to attenuate Ang II-induced LV hypertrophy using a 9.4T pre-clinical magnetic resonance imaging instrument |
Since they didn’t perform electrocardiography, they were unable to confirm the superiority of MRI in assessing cardiac remodeling |
Gao Q. et al. (2020)
|
Thromboxane A2 (TP) knockout (Tp−/−) mice |
1,000 ng/kg/min, s.c., 28 days |
TP receptors may contribute to cardiac hypertrophy but not, proteinuria and are responsible for thepathogenesis of Ang II induced hypertension and hypertrophy |
As thromboxane production was not analyzed in Cox1−/− mice, they were unable to assure the reduction caused by TXA2 |
Heo et al. (2019)
|
Sprague-Dawley rats |
200 ng/kg/min, micro-infusion |
Ghrelin inhibited Ang II-induced cardiac fibrosisin a PPAR-dependent manner |
The study was performed on young male rats which restricts the extrapolation of results for females and older cohorts. |
Zhong et al. (2018)
|
Also, the age and sex-mediated effects of ghrelin need to be explored. |
Rat tubular epithelial cell line NRK52E |
1 mM for 0–24 h |
Inhibition of HMGB1 and gene silencing of TLR4 decreases Ang II-mediated inflammation in the kidney |
Future in-vivo studies will be required for elucidating the role of TLR4 signaling in Ang II-induced renal injury on the AT1 R knock out model |
Nair et al. (2015)
|
The existence of HMGB1-TLR4 signaling is a development of hypertensive renal injury |
Mouse Neuro-2a cells |
- |
Involvement of HMGB1 in the PVN for development of Ang II-induced hypertension |
Further research depicting the involvement of Mas will be necessary |
Nair and Philips, (2015)
|
Sprague-Dawley rats |
120 ng/kg/min, s.c.,2 weeks |
Activation of brain RAS and PPAR-γ to reduce central inflammation may be used as a strategy in the management of Ang II-induced hypertension |
Studies need to be performed to evaluate the relative role of individual types of cell |
Yu et al. (2015)
|
Sprague-Dawley rats |
100 ng/kg, i. c. v., before and after a 1 h ICV infusion of inhibitor |
Role of brain p44/42 MAPK signaling cascade in the maintenance of renal sympathetic excitation in HF rats. |
They evaluated the involvement of p44/42 MAPK signaling in the brain containing presympathetic neurons of PVN neurons only and did not evidence the contribution of p44/42 MAPK signaling in other nuclei of brain-like RVLM or other neurons in cardiovascular and autonomic centers, including organum vasculosum of the lamina terminalis, median preoptic nucleus, and the subfornical organ. |
Shinohara et al. (2015)
|
Alteration in brain p44/42 MAPK can increase adverse effects of brain RAS on renal and cardiovascular functions during HF progression. |
Attenuation in Fra-LI–positive PVN neurons in p44/42 MAPK inhibitors treated rats suffering from HF. |
Sprague-Dawley rats |
800 ng/kg/min, s.c., 1 week |
Association of NO-mediated mechanisms with presence of female sex hormones to be protective against sympathetically mediated Ang II-induced hypertension in female mice |
- |
Wattanapitayakul et al. (2000)
|