TRPC Channels As Effectors of Cardiac Hypertrophy

@article{Eder2011TRPCCA,
  title={TRPC Channels As Effectors of Cardiac Hypertrophy},
  author={Petra Eder and Jeffery D. Molkentin},
  journal={Circulation Research},
  year={2011},
  volume={108},
  pages={265–272}
}
Transient receptor potential (TRP) channels of multiple subclasses are expressed in the heart, although their functions are only now beginning to emerge, especially for the TRPC subclass that appears to regulate the cardiac hypertrophic response. Although TRP channels permeate many different cations, they are most often ascribed a specific biological function because of Ca2+ influx, either for microdomain signaling or to reload internal Ca2+ stores in the endoplasmic reticulum through a store… 

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References

SHOWING 1-10 OF 85 REFERENCES
TRPC channels are necessary mediators of pathologic cardiac hypertrophy
TLDR
Three dn transgenic strategies attenuated the cardiac hypertrophic response following either neuroendocrine agonist infusion or pressure-overload stimulation, and dnTRPC4 inhibited the activity of the TRPC3/6/7 subfamily in the heart, suggesting that these two subfamilies function in coordinated complexes.
Canonical Transient Receptor Potential Channels Promote Cardiomyocyte Hypertrophy through Activation of Calcineurin Signaling*
TLDR
A novel role for TRPC channels is defined in the control of cardiac growth, and it is suggested that a TRPC-derived pool of calcium contributes to selective activation of calcineurin in diseased heart.
TRPC1 Channels Are Critical for Hypertrophic Signaling in the Heart
TLDR
It is suggested that TRPC1 channels are critical for the adaptation to biomechanical stress and TRPC dysregulation leads to maladaptive cardiac hypertrophy and failure.
Upregulation of TRPC1 in the development of cardiac hypertrophy.
Increased Vascular Smooth Muscle Contractility in TRPC6−/− Mice
TLDR
It is implied that constitutively active TRPC3-type channels, which are up-regulated in TRPC6-deficient smooth muscle cells, are not able to functionally replace TRPC 6, which has distinct nonredundant roles in the control of vascular smooth muscle tone.
TRPC6 fulfills a calcineurin signaling circuit during pathologic cardiac remodeling.
TLDR
Cardiac-specific overexpression of TRPC6 in transgenic mice resulted in heightened sensitivity to stress, a propensity for lethal cardiac growth and heart failure, and an increase in NFAT-dependent expression of beta-myosin heavy chain, a sensitive marker for pathologic hypertrophy.
Transient Receptor Potential Canonical Type 1 (TRPC1) Operates as a Sarcoplasmic Reticulum Calcium Leak Channel in Skeletal Muscle*
TLDR
The functional role of TRPC1 is investigated using an overexpressing strategy in adult mouse muscle fibers to demonstrate that it operates as a SR Ca2+ leak channel in skeletal muscle.
TRPC3 channels colocalize with Na+/Ca2+ exchanger and Na+ pump in axial component of transverse-axial tubular system of rat ventricle.
TLDR
Results suggest that TRPC3 is localized in the ventricular myocyte to the axial component of the transverse-axial tubular system, where it exists in a signaling complex that includes NCX and NKA.
Regulation of canonical transient receptor potential isoform 3 (TRPC3) channel by protein kinase G.
  • H. KwanYu HuangX. Yao
  • Biology, Chemistry
    Proceedings of the National Academy of Sciences of the United States of America
  • 2004
TLDR
Taken together, TRPC3 channels could be directly phosphorylated by PKG at position T11 and S263, and this phosphorylation abolished the store-operated Ca2+ influx mediated by TR PC3 channels in HEK293 cells.
The pathological role of transient receptor potential channels in heart disease.
TLDR
Evidence suggests that upregulation of TRPC channels is involved in the development of cardiac hypertrophy and heart failure and some TRP channels with anticipated roles in disease might become novel pharmacological targets in the treatment of human heart disease.
...
...