Mas receptor: a potential strategy in the management of ischemic cardiovascular diseases

Molaei, Ali; Molaei, Emad; Hayes, A. Wallace; Karimi, Gholamreza

doi:10.1080/15384101.2023.2228089

Cited by 10 publications

(2 citation statements)

References 163 publications

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“…Formed kallikrein cleaves HK to liberate BK [20]. Activation of the BKB2 (B 2 ) receptors [21] by BK and the Mas oncogene receptors [22] by Ang1-7 lead, among others, to vasorelaxation and improving cell metabolism via the generation of nitric oxide (NO), which was found to prevent endothelial senescence [23]. Strikingly, it is controversial as to whether Ang 1-7 mediates its effect via the proto-oncogene Mas receptors [24].…”

Section: Introductionmentioning

confidence: 99%

Increased Prolylcarboxypeptidase Expression Can Serve as a Biomarker of Senescence in Culture

Boullard,

Paris,

Shariat-Madar

et al. 2024

Molecules

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Prolylcarboxypeptidase (PRCP, PCP, Lysosomal Pro-X-carboxypeptidase, Angiotensinase C) controls angiotensin- and kinin-induced cell signaling. Elevation of PRCP appears to be activated in chronic inflammatory diseases [cardiovascular disease (CVD), diabetes] in proportion to severity. Vascular endothelial cell senescence and mitochondrial dysfunction have consistently been shown in models of CVD in aging. Cellular senescence, a driver of age-related dysfunction, can differentially alter the expression of lysosomal enzymes due to lysosomal membrane permeability. There is a lack of data demonstrating the effect of age-related dysfunction on the expression and function of PRCP. To explore the changes in PRCP, the PRCP-dependent prekallikrein (PK) pathway was characterized in early- and late-passage human pulmonary artery endothelial cells (HPAECs). Detailed kinetic analysis of cells treated with high molecular weight kininogen (HK), a precursor of bradykinin (BK), and PK revealed a mechanism by which senescent HPAECs activate the generation of kallikrein upon the assembly of the HK–PK complex on HPAECs in parallel with an upregulation of PRCP and endothelial nitric oxide (NO) synthase (eNOS) and NO formation. The NO production and expression of both PRCP and eNOS increased in early-passage HPAECs and decreased in late-passage HPAECs. Low activity of PRCP in late-passage HPAECs was associated with rapid decreased telomerase reverse transcriptase mRNA levels. We also found that, with an increase in the passage number of HPAECs, reduced PRCP altered the respiration rate. These results indicated that aging dysregulates PRCP protein expression, and further studies will shed light into the complexity of the PRCP-dependent signaling pathway in aging.

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Section: Introductionmentioning

confidence: 99%

Increased Prolylcarboxypeptidase Expression Can Serve as a Biomarker of Senescence in Culture

Boullard,

Paris,

Shariat-Madar

et al. 2024

Molecules

View full text Add to dashboard Cite

show abstract

“…Formed kallikrein cleaves HK to liberate BK [20]. Activation of the BKB2 (B2) receptors [21] by BK and the Mas oncogene receptors [22] by Ang1-7 lead, among others, to vasorelaxation and improving cell metabolism via the generation of nitric oxide (NO), which was found to prevent endothelial senescence [23]. Strikingly, it is controversial as to whether Ang 1-7 mediates its effect via the proto-oncogene Mas receptors [24].…”

Section: Introductionmentioning

confidence: 99%

Increased Prolylcarboxypeptidase Expression Can Serve as Biomarker of Senescence in Culture

Boullard,

Paris,

Shariat-Madar

et al. 2024

Preprint

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Prolylcarboxypeptidase (PRCP, PCP, Lysosomal Pro-X-carboxypeptidase, Angiotensinase C) controls angiotensin - and kinin- induced cell signaling. Elevation of PRCP appear to be activated in chronic inflammatory diseases (cardiovascular disease (CVD), diabetes) in proportion to severity. Vascular endothelial cell senescence and mitochondrial dysfunction have consistently been shown in models of CVD in aging. The cellular senescence, a driver of age-related dysfunction, can differentially alter the expression of lysosomal enzymes due to lysosomal membrane permeability. There is a lack of data demostrating the effect of age-related dysfunction on the expression and function of PRCP. To explore the changes in PRCP, PRCP-dependent prekallikrein (PK) pathway was charcterized in early – and late-passage human pulmonary artery endothelial cells (HPAECs). Detailed kinetic analysis of cells treated with high molecular weight kininogen (HK), a precursor of bradykinin (BK), and PK revealed a mechansim by which senescent HPAECs activate the generation of kallikrein upon the assembly of the HK-PK complex on HPAECs in parallel with an upregulation of PRCP and endothelial nitric oxide (NO) synthase (eNOS) and NO formation. The NO production and expression of both PRCP and eNOS increased in early-passage HPAECs while decreased in late-passage HPAECs. Low activity of PRCP in late passage HPAECs was associated with rapid decreased telomerase reverse transcriptase mRNA levels. We also found that, with an increase in the passage number of HPAECs, reduced PRCP altered respiration rate. These results indicated that aging dysregulates PRCP protein expression, and further studies will shed light into the complexity of PRCP-dependent signling pathway in aging.

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The Cardiovascular Protective Function of Natural Compounds Through AMPK/SIRT1/PGC‐1α Signaling Pathway

Rahmani,

Roohbakhsh,

Pourbarkhordar

et al. 2024

Food Science & Nutrition

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Cardiovascular disease (CVD) poses a major risk to human health and exert a heavy burden on individuals, society, and healthcare systems. Therefore, it is critical to identify CVD's underlying mechanism(s) and target them using effective agents. Natural compounds have shown promise as antioxidants with cardioprotective functions against CVD injuries due to their antioxidative solid capacity and high safety profile. Several CVDs, such as heart failure, ischemia/reperfusion, atherosclerosis, and cardiomyopathies, are closely linked to mitochondrial dysfunction. It is well established that activating the AMPK/SIRT1/PGC‐1α pathway during CVD promotes mitochondrial function. Therefore, targeting the AMPK/SIRT1/PGC‐1α pathway provides a foundation for novel therapeutic strategies to combat CVD. A key goal of our search was to find natural compounds that target this biological pathway and have beneficial effects on CVD.

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Mas receptor: a potential strategy in the management of ischemic cardiovascular diseases

Cited by 10 publications

References 163 publications

Increased Prolylcarboxypeptidase Expression Can Serve as a Biomarker of Senescence in Culture

Increased Prolylcarboxypeptidase Expression Can Serve as a Biomarker of Senescence in Culture

Increased Prolylcarboxypeptidase Expression Can Serve as Biomarker of Senescence in Culture

The Cardiovascular Protective Function of Natural Compounds Through AMPK/SIRT1/PGC‐1α Signaling Pathway

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