Cathepsins in heart disease–chewing on the heartache?
Key result
Cathepsin B knockout or pharmacological inhibition attenuates pressure overload-induced cardiac hypertrophy and apoptosis via the TNF-α/ASK1/JNK signaling pathway in experimental models.
Why the study?
Does Cathepsin B inhibition prevent cardiac remodeling and hypertrophy in preclinical models of pressure overload?
Population
Preclinical models: mice subjected to transaortic constriction for up to 8 weeks, and H9c2 rat myoblastic…
Comparison
Cathepsin B knockout, shRNA knockdown, or… vs Wild-type (WT) littermates or control cells
Design
Editorial
Follow-up
up to 8 wk
Authors
Discussion
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Implication
This editorial highlights preclinical evidence that cathepsin B plays a necessary role in pressure overload-induced cardiac remodeling and apoptosis via the TNF-α/ASK1/JNK pathway.
Structured PICO
Does Cathepsin B inhibition prevent cardiac remodeling and hypertrophy in preclinical models of pressure overload?
P
Population
Preclinical models: mice subjected to transaortic constriction (TAC) for up to 8 weeks, and H9c2 rat myoblastic cells stimulated with ANG II
I
Intervention
Cathepsin B (CTSB) knockout, shRNA knockdown, or pharmacologic inhibition (CA-074Me)
C
Comparator
Wild-type (WT) littermates or control cells
O
Outcome
Cardiac hypertrophy, fibrosis, and apoptosissurrogate
This editorial highlights preclinical evidence that cathepsin B plays a necessary role in pressure overload-induced cardiac remodeling and apoptosis via the TNF-α/ASK1/JNK pathway.
Limitations
- Systemic administration of cathepsin inhibitors has high potential for side-effects and cytotoxicity due to ubiquitous tissue expression.
- Differences exist between CTSB and NLRP3 knockout models post-TAC, warranting further study.
Cite This Study
Blondelle et al. (2015) conducted an editorial in Cardiac remodeling. Cathepsin B inhibition or knockout was evaluated. Cathepsin B knockout or pharmacological inhibition attenuates pressure overload-induced cardiac hypertrophy and apoptosis via the TNF-α/ASK1/JNK signaling pathway in experimental models.