Difference between revisions of "Li 2022 Hypertens Res"
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{{Publication | {{Publication | ||
|title=Li L, Ma L, Luo Z, Wei X, Zhao Y, Zhou C, Mou A, Lu Z, You M, He C, Ma H, Zhou Q, Wang L, Cao T, Gu Y, Gao P, Zhu Z (2022) Lack of TRPV1 aggravates obesity-associated hypertension through the disturbance of mitochondrial | |title=Li L, Ma L, Luo Z, Wei X, Zhao Y, Zhou C, Mou A, Lu Z, You M, He C, Ma H, Zhou Q, Wang L, Cao T, Gu Y, Gao P, Zhu Z (2022) Lack of TRPV1 aggravates obesity-associated hypertension through the disturbance of mitochondrial Ca<sup>2+</sup> homeostasis in brown adipose tissue. Hypertens Res [Epub ahead of print]. | ||
|info=[https://www.ncbi.nlm.nih.gov/pubmed/35043013 PMID: 35043013 Open Access] | |info=[https://www.ncbi.nlm.nih.gov/pubmed/35043013 PMID: 35043013 Open Access] | ||
|authors=Li L, Ma L, Luo Z, Wei X, Zhao Y, Zhou C, Mou A, Lu Z, You M, He C, Ma H, Zhou Q, Wang L, Cao T, Gu Y, Gao P, Zhu Z | |authors=Li L, Ma L, Luo Z, Wei X, Zhao Y, Zhou C, Mou A, Lu Z, You M, He C, Ma H, Zhou Q, Wang L, Cao T, Gu Y, Gao P, Zhu Z | ||
|year=2022 | |year=2022 | ||
|journal=Hypertens Res | |journal=Hypertens Res | ||
|abstract=The combination of obesity and hypertension is associated with high morbidity and mortality; however, the mechanism underlying obesity-induced hypertension remains unclear. In this study, we detected the possible effects of TRPV1, a previously identified antihypertensive calcium ( | |abstract=The combination of obesity and hypertension is associated with high morbidity and mortality; however, the mechanism underlying obesity-induced hypertension remains unclear. In this study, we detected the possible effects of TRPV1, a previously identified antihypertensive calcium (Ca<sup>2+</sup>) channel in adipose tissue, on the occurrence of obesity and hypertension in mice lacking UCP1, a spontaneously genetically manipulated obesity model, by generating TRPV1 and UCP1 double knockout mice. In these mice, obesity and hypertension appeared earlier and were more severe than in mice with the knockout of UCP1 or TRPV1 alone. The knockout of TRPV1 in UCP1 knockout mice further reduced functional brown adipose tissue (BAT) generation; decreased resting oxygen consumption, heat production, and locomotor activities; and was accompanied by severe mitochondrial respiratory dysfunction in BAT. Mechanistically, TRPV1, UCP1, and LETM1 acted as a complex to maintain an appropriate mitochondrial Ca<sup>2+</sup> level, and TRPV1 knockout caused a compensatory increase in mitochondrial Ca<sup>2+</sup> uptake via LETM1 activation. However, the compensatory response was blocked in UCP1<sup>-/-</sup> mice, resulting in dramatically reduced mitochondrial Ca<sup>2+</sup> uptake and higher production of ATP and oxidative stress. This study provides ''in vivo'' evidence for the critical role of BAT mitochondrial Ca<sup>2+</sup> homeostasis in obesity-associated hypertension and indicates that the TRPV1/UCP1/LETM1 complex may be an alternative intervention target. | ||
|editor=[[Plangger M]] | |editor=[[Plangger M]] | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration, Genetic knockout;overexpression | ||
|organism=Mouse | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=2022-01 | |additional=2022-01 | ||
}} | }} | ||
Revision as of 19:35, 24 January 2022
| Li L, Ma L, Luo Z, Wei X, Zhao Y, Zhou C, Mou A, Lu Z, You M, He C, Ma H, Zhou Q, Wang L, Cao T, Gu Y, Gao P, Zhu Z (2022) Lack of TRPV1 aggravates obesity-associated hypertension through the disturbance of mitochondrial Ca2+ homeostasis in brown adipose tissue. Hypertens Res [Epub ahead of print]. |
Li L, Ma L, Luo Z, Wei X, Zhao Y, Zhou C, Mou A, Lu Z, You M, He C, Ma H, Zhou Q, Wang L, Cao T, Gu Y, Gao P, Zhu Z (2022) Hypertens Res
Abstract: The combination of obesity and hypertension is associated with high morbidity and mortality; however, the mechanism underlying obesity-induced hypertension remains unclear. In this study, we detected the possible effects of TRPV1, a previously identified antihypertensive calcium (Ca2+) channel in adipose tissue, on the occurrence of obesity and hypertension in mice lacking UCP1, a spontaneously genetically manipulated obesity model, by generating TRPV1 and UCP1 double knockout mice. In these mice, obesity and hypertension appeared earlier and were more severe than in mice with the knockout of UCP1 or TRPV1 alone. The knockout of TRPV1 in UCP1 knockout mice further reduced functional brown adipose tissue (BAT) generation; decreased resting oxygen consumption, heat production, and locomotor activities; and was accompanied by severe mitochondrial respiratory dysfunction in BAT. Mechanistically, TRPV1, UCP1, and LETM1 acted as a complex to maintain an appropriate mitochondrial Ca2+ level, and TRPV1 knockout caused a compensatory increase in mitochondrial Ca2+ uptake via LETM1 activation. However, the compensatory response was blocked in UCP1-/- mice, resulting in dramatically reduced mitochondrial Ca2+ uptake and higher production of ATP and oxidative stress. This study provides in vivo evidence for the critical role of BAT mitochondrial Ca2+ homeostasis in obesity-associated hypertension and indicates that the TRPV1/UCP1/LETM1 complex may be an alternative intervention target.
• Bioblast editor: Plangger M
Labels: MiParea: Respiration, Genetic knockout;overexpression
Organism: Mouse
HRR: Oxygraph-2k
2022-01
