What is the clinical evidence from this study?

Study design: Other. Population: Obesity-induced arterial stiffening. Intervention: Pioglitazone (PPARγ agonist). Primary outcome: Arterial stiffening and PVAT microenvironment (expression of pro-inflammatory and pro-oxidative factors, elastin fiber fragmentation, elastolytic activity).

March 29, 2021Journal of Biomedical ScienceOpen Access

PPARγ activation improves the microenvironment of perivascular adipose tissue and attenuates aortic stiffening in obesity

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Key result

Pioglitazone attenuates obesity-induced arterial stiffening in mice by reducing PVAT inflammation and oxidative stress.

Why the study?

Current therapies for arterial stiffening do not directly target the vessel, and whether PPARγ activation attenuates obesity-related arterial stiffening by altering the perivascular adipose tissue microenvironment was unknown.

Does pioglitazone improve the perivascular adipose tissue microenvironment and attenuate aortic stiffening in obese ob/ob mice?

Population

Obese ob/ob mice and vascular/adipose-related cell types

Comparison

PPARγ activation with pioglitazone vs controls

Design

Preclinical animal and in vitro study

Authors

JCJu‐Yi Chen YWYipin Wu CLChih-Yi Li

Discussion

Member takes

Overview

Should not change practice in obese patients; hypothesis-generating for PPARγ activation in human arterial stiffness.

Key Points

To determine whether PPARγ activation improves the microenvironment of perivascular adipose tissue to attenuate obesity-induced arterial stiffening.
Treated obese ob/ob mice with the PPARγ agonist pioglitazone to measure changes in arterial stiffness and perivascular adipose tissue biology.
Assayed elastolytic enzyme expression and direct PPARγ gene binding across macrophages, fibroblasts, adipocytes, and vascular smooth muscle cells.
Pioglitazone significantly attenuated arterial stiffening in ob/ob mice, driven by an improved perivascular adipose tissue microenvironment with reduced pro-inflammatory and pro-oxidative factors rather than fat browning.
Treatment suppressed obesity-induced elastin fiber fragmentation and elastolytic activity by downregulating cathepsin S and metalloproteinase 12 predominantly in perivascular adipose tissue.
Direct PPARγ binding sites were identified on Ctss and Mmp12 genes in Raw 264.7 and 3T3-L1 cells, confirming a direct transcriptional repression mechanism in macrophages and fibroblasts.

Structured PICO

Does pioglitazone improve the perivascular adipose tissue microenvironment and attenuate aortic stiffening in obese ob/ob mice?

Population

Obese ob/ob mice and in vitro cell models (macrophages, fibroblasts, adipocytes, vascular smooth muscle cells, Raw 264.7, and 3T3-L1 cells)

Intervention

Pioglitazone (PPARγ agonist)

Outcome

Arterial stiffening and perivascular adipose tissue (PVAT) microenvironment changessurrogate

PPARγ activation with pioglitazone attenuates obesity-induced arterial stiffening by improving the perivascular adipose tissue microenvironment and reducing elastolytic activity.

Cite This Study

Chen et al. (2021) studied Obesity-induced arterial stiffening. Pioglitazone (PPARγ agonist) was evaluated on Arterial stiffening and PVAT microenvironment (expression of pro-inflammatory and pro-oxidative factors, elastin fiber fragmentation, elastolytic activity). PPARγ activation by pioglitazone attenuated obesity-induced arterial stiffening and reduced the inflammatory and oxidative status of perivascular adipose tissue in ob/ob mice.

synapsesocial.com/papers/6a0932ef4c1e2db30bd26506 https://doi.org/10.1186/s12929-021-00720-y

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March 29, 2021Journal of Biomedical ScienceOpen Access

PPARγ activation improves the microenvironment of perivascular adipose tissue and attenuates aortic stiffening in obesity

View Full Paper

Ask AI

Bookmark

Key result

Pioglitazone attenuates obesity-induced arterial stiffening in mice by reducing PVAT inflammation and oxidative stress.

Why the study?

Does pioglitazone improve the perivascular adipose tissue microenvironment and attenuate aortic stiffening in obese ob/ob mice?

Population

Obese ob/ob mice and vascular/adipose-related cell types

Comparison

PPARγ activation with pioglitazone vs controls

Design

Preclinical animal and in vitro study

Authors

JCJu‐Yi Chen YWYipin Wu CLChih-Yi Li

Discussion

Member takes

Overview

Should not change practice in obese patients; hypothesis-generating for PPARγ activation in human arterial stiffness.

Key Points

To determine whether PPARγ activation improves the microenvironment of perivascular adipose tissue to attenuate obesity-induced arterial stiffening.
Treated obese ob/ob mice with the PPARγ agonist pioglitazone to measure changes in arterial stiffness and perivascular adipose tissue biology.
Assayed elastolytic enzyme expression and direct PPARγ gene binding across macrophages, fibroblasts, adipocytes, and vascular smooth muscle cells.
Pioglitazone significantly attenuated arterial stiffening in ob/ob mice, driven by an improved perivascular adipose tissue microenvironment with reduced pro-inflammatory and pro-oxidative factors rather than fat browning.
Treatment suppressed obesity-induced elastin fiber fragmentation and elastolytic activity by downregulating cathepsin S and metalloproteinase 12 predominantly in perivascular adipose tissue.
Direct PPARγ binding sites were identified on Ctss and Mmp12 genes in Raw 264.7 and 3T3-L1 cells, confirming a direct transcriptional repression mechanism in macrophages and fibroblasts.

Structured PICO

Does pioglitazone improve the perivascular adipose tissue microenvironment and attenuate aortic stiffening in obese ob/ob mice?

Population

Obese ob/ob mice and in vitro cell models (macrophages, fibroblasts, adipocytes, vascular smooth muscle cells, Raw 264.7, and 3T3-L1 cells)

Intervention

Pioglitazone (PPARγ agonist)

Outcome

Arterial stiffening and perivascular adipose tissue (PVAT) microenvironment changessurrogate

PPARγ activation with pioglitazone attenuates obesity-induced arterial stiffening by improving the perivascular adipose tissue microenvironment and reducing elastolytic activity.

Cite This Study

synapsesocial.com/papers/6a0932ef4c1e2db30bd26506 https://doi.org/10.1186/s12929-021-00720-y

Also Consider

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