What is the clinical evidence from this study?

Study design: Other. Population: Diabetic cardiomyopathy. Intervention: rAAV-miR-30c vs. rAAV-miR-random. Primary outcome: Cardiac dysfunction and metabolic derangement (p=<0.05).

What does this research mean for the field?

Overexpression of miR-30c protects against diabetic cardiomyopathy by targeting PGC-1β and reducing PPARα transcriptional activity, which attenuates cardiomyocyte apoptosis and cardiac dysfunction. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

January 11, 2019Cardiovascular DiabetologyOpen Access

Overexpression of miR-30c by rAAV system attenuated cardiomyocyte apoptosis and cardiac dysfunction in db/db mice by targeting PGC-1β and reducing PPARα transcriptional activity.

Q: What are the key findings of this study?

Q: What does this research mean for the field?

Overexpression of miR-30c protects against diabetic cardiomyopathy by targeting PGC-1β and reducing PPARα transcriptional activity, which attenuates cardiomyocyte apoptosis and cardiac dysfunction. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

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Why the study?

Metabolic abnormalities are implicated as a causal event in diabetic cardiomyopathy, but the mechanisms underlying cardiac metabolic disorder were not fully understood.

Population

Db/db mice, palmitate-treated H9c2 cells, and primary neonatal rat cardiomyocytes

Design

Preclinical laboratory and animal study

Key result

Overexpression of miR-30c by rAAV system attenuated cardiomyocyte apoptosis and cardiac dysfunction in db/db mice by targeting PGC-1β and reducing PPARα transcriptional activity.

Authors

ZYZhongwei Yin YZYanru Zhao MHMengying He

Discussion

Member takes

Overview

Supports miR-30c targeting in diabetic cardiomyopathy models; hypothesis-generating and requires human validation before clinical consideration.

Structured PICO

Population

Male db/db mice with C57BL/Ks background (n=8-10 per group), palmitate-treated H9c2 cells, and primary neonatal rat cardiomyocytes.

Intervention

rAAV9-mediated overexpression of miR-30c (in vivo) or miR-30c mimics / PGC-1β siRNA (in vitro).

Comparator

rAAV-miR-random (in vivo), miR-con or si-con (in vitro), and non-diabetic C57BL/Ks control mice.

Outcome

Cardiac metabolism, lipotoxicity, reactive oxygen species production, cardiomyocyte apoptosis, and cardiac dysfunction.surrogate

Main Result

p-value: p=<0.05

miR-30c protects against diabetic cardiomyopathy by targeting PGC-1β and reducing PPARα transcriptional activity, suggesting a potential therapeutic target.

Limitations

Whether other transcriptional factors are involved in PGC-1β induced metabolic disorder needs further study
The involvement of miR-30c/PGC-1β in regulating mitochondrial biogenesis needs further study

Cite This Study

Yin et al. (2019) studied Diabetic cardiomyopathy. rAAV-miR-30c vs. rAAV-miR-random was evaluated on Cardiac dysfunction and metabolic derangement (p=<0.05). Overexpression of miR-30c by rAAV system attenuated cardiomyocyte apoptosis and cardiac dysfunction in db/db mice by targeting PGC-1β and reducing PPARα transcriptional activity.

synapsesocial.com/papers/6a178aa08d470cd99253614f https://doi.org/10.1186/s12933-019-0811-7

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January 11, 2019Cardiovascular DiabetologyOpen Access

Overexpression of miR-30c by rAAV system attenuated cardiomyocyte apoptosis and cardiac dysfunction in db/db mice by targeting PGC-1β and reducing PPARα transcriptional activity.

View Full Paper

Ask AI

Bookmark

Why the study?

Metabolic abnormalities are implicated as a causal event in diabetic cardiomyopathy, but the mechanisms underlying cardiac metabolic disorder were not fully understood.

Population

Db/db mice, palmitate-treated H9c2 cells, and primary neonatal rat cardiomyocytes

Design

Preclinical laboratory and animal study

Key result

Overexpression of miR-30c by rAAV system attenuated cardiomyocyte apoptosis and cardiac dysfunction in db/db mice by targeting PGC-1β and reducing PPARα transcriptional activity.

Authors

ZYZhongwei Yin YZYanru Zhao MHMengying He

Discussion

Member takes

Overview

Supports miR-30c targeting in diabetic cardiomyopathy models; hypothesis-generating and requires human validation before clinical consideration.

Structured PICO

Population

Male db/db mice with C57BL/Ks background (n=8-10 per group), palmitate-treated H9c2 cells, and primary neonatal rat cardiomyocytes.

Intervention

rAAV9-mediated overexpression of miR-30c (in vivo) or miR-30c mimics / PGC-1β siRNA (in vitro).

Comparator

rAAV-miR-random (in vivo), miR-con or si-con (in vitro), and non-diabetic C57BL/Ks control mice.

Outcome

Cardiac metabolism, lipotoxicity, reactive oxygen species production, cardiomyocyte apoptosis, and cardiac dysfunction.surrogate

Main Result

p-value: p=<0.05

miR-30c protects against diabetic cardiomyopathy by targeting PGC-1β and reducing PPARα transcriptional activity, suggesting a potential therapeutic target.

Limitations

Whether other transcriptional factors are involved in PGC-1β induced metabolic disorder needs further study
The involvement of miR-30c/PGC-1β in regulating mitochondrial biogenesis needs further study

Cite This Study

synapsesocial.com/papers/6a178aa08d470cd99253614f https://doi.org/10.1186/s12933-019-0811-7

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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