What does this research mean for the field?

Doxorubicin-induced cardiomyopathy is mechanistically driven by peroxynitrite-related protein nitration, which selectively targets and inactivates myofibrillar creatine kinase (MM-CK) in the cardiac contractile apparatus. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

February 1, 2002British Journal of PharmacologyOpen Access

Intracellular distribution of peroxynitrite during doxorubicin cardiomyopathy: evidence for selective impairment of myofibrillar creatine kinase

View Full Paper

Ask AI

Bookmark

Population

Mice and skinned ventricular trabeculae

Comparison

Doxorubicin in vivo; peroxynitrite in vitro vs Vehicle control

Design

Preclinical

Follow-up

5 days (in vivo)

Authors

MMMichael J. MihmThe Ohio State University FYFushun YuChina Medical University DWDavid M. WeinsteinColorado Engineering (United States)

Discussion

Member takes

Implication

Peroxynitrite-mediated MM-CK inactivation may contribute to doxorubicin cardiotoxicity; hypothesis-generating in animals, clinical relevance remains open.

Structured PICO

Population

Mice and skinned ventricular trabeculae

Intervention

Doxorubicin (20 mg/kg) in vivo; peroxynitrite (50 or 300 nM) in vitro

Comparator

Vehicle control

Outcome

Intracellular distribution of 3-nitrotyrosine and myofibrillar creatine kinase (MM-CK) activitysurrogate

Peroxynitrite-related protein nitration, specifically targeting myofibrillar creatine kinase, is a key mechanistic event in doxorubicin-induced cardiomyopathy.

Cite This Study

Mihm et al. (2002) studied this question.

synapsesocial.com/papers/6a1bd672ea84844e355f0d92 https://doi.org/10.1038/sj.bjp.0704495

Topics

Cardiomyopathy

View Full Paper

Ask AI

Bookmark

February 1, 2002British Journal of PharmacologyOpen Access

Intracellular distribution of peroxynitrite during doxorubicin cardiomyopathy: evidence for selective impairment of myofibrillar creatine kinase

View Full Paper

Ask AI

Bookmark

Population

Mice and skinned ventricular trabeculae

Comparison

Doxorubicin in vivo; peroxynitrite in vitro vs Vehicle control

Design

Preclinical

Follow-up

5 days (in vivo)

Authors

MMMichael J. MihmThe Ohio State University FYFushun YuChina Medical University DWDavid M. WeinsteinColorado Engineering (United States)

Discussion

Member takes

Implication

Peroxynitrite-mediated MM-CK inactivation may contribute to doxorubicin cardiotoxicity; hypothesis-generating in animals, clinical relevance remains open.

Structured PICO

Population

Mice and skinned ventricular trabeculae

Intervention

Doxorubicin (20 mg/kg) in vivo; peroxynitrite (50 or 300 nM) in vitro

Comparator

Vehicle control

Outcome

Intracellular distribution of 3-nitrotyrosine and myofibrillar creatine kinase (MM-CK) activitysurrogate

Peroxynitrite-related protein nitration, specifically targeting myofibrillar creatine kinase, is a key mechanistic event in doxorubicin-induced cardiomyopathy.

Cite This Study

Mihm et al. (2002) studied this question.

synapsesocial.com/papers/6a1bd672ea84844e355f0d92 https://doi.org/10.1038/sj.bjp.0704495

Also Consider

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

Topics

Cardiomyopathy

View Full Paper

Ask AI

Bookmark