What is the clinical evidence from this study?

Study design: Other. Population: TNF-induced myocardial inflammation (n=8). Intervention: TNFR1 knockout vs. Wild-type (WT). Primary outcome: SOCS3 expression (percentage of SOCS3/GAPDH).

November 18, 2006AJP Heart and Circulatory PhysiologyOpen Access

Deficiency of TNFR1 protects myocardium through SOCS3 and IL-6 but not p38 MAPK or IL-1β

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Key result

TNFR1 deficiency in isolated mouse hearts subjected to TNF infusion resulted in significantly greater SOCS3 expression (45% vs 22%) and decreased IL-6 production.

Population

Isolated male mouse hearts from wild-type (WT) and TNFR1 knockout (TNFR1KO) mice (n = 4/group)

Comparison

TNFR1 deficiency subjected to direct TNF… vs Wild-type hearts subjected to the same direct…

Design

Preclinical

Follow-up

30 minutes

Authors

MWMeijing WangZhejiang Sci-Tech University TMTroy A. MarkelPurdue University West Lafayette PCPaul R. CrisostomoLoyola University Medical Center

Discussion

Member takes

Implication

Hypothesis-generating for TNFR1 modulation in TNF-driven myocardial injury; leaves open translation to human cardiac disease.

Structured PICO

Population

8 isolated male mouse hearts (n=4/group) from wild-type and TNFR1 knockout mice subjected to direct TNF infusion.

Intervention

TNFR1 deficiency (TNFR1KO) subjected to direct TNF infusion (500 pg.ml(-1).min(-1) x 30 min)

Comparator

Wild-type (WT) hearts subjected to the same direct TNF infusion

Outcome

Myocardial function (left ventricular developed pressure and maximal positive/negative dP/dt), myocardial LDH release, and expression of SOCS3, STAT3, IL-6, p38, and IL-1betasurrogate

Main Result

Absolute Event Rate: 45% vs 22%

TNFR1 deficiency protects myocardial function and reduces inflammation in response to TNF via the SOCS3 and IL-6 pathways, suggesting a potential mechanism for mitigating TNF-induced myocardial injury.

Cite This Study

Wang et al. (2006) studied TNF-induced myocardial inflammation (n=8). TNFR1 knockout vs. Wild-type (WT) was evaluated on SOCS3 expression (percentage of SOCS3/GAPDH). TNFR1 deficiency in isolated mouse hearts subjected to TNF infusion resulted in significantly greater SOCS3 expression (45% vs 22%) and decreased IL-6 production.

synapsesocial.com/papers/6a7474ff0081fe7b05dbd52f https://doi.org/10.1152/ajpheart.01063.2006

Topics

Myocarditis

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Deficiency of TNFR1 protects myocardium through SOCS3 and IL-6 but not p38 MAPK or IL-1β

Discussion

Member takes

Implication

Structured PICO

Main Result

Cite This Study

Topics

Deficiency of TNFR1 protects myocardium through SOCS3 and IL-6 but not p38 MAPK or IL-1β

Discussion

Member takes

Implication

Structured PICO

Main Result

Cite This Study

Also Consider

Topics

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