ReviewHeart failure reviews2000
Cardiocyte cytoskeleton in hypertrophied myocardium.
Review in Heart failure reviews, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 49 citations in OpenAlex.
- The microtubule cytoskeleton in cardiac mechanics and heart failure.Nature reviews. Cardiology · 2022Review
- Cardiomyocyte Microtubules: Control of Mechanics, Transport, and Remodeling.Annual review of physiology · 2022Review
- A guide for assessment of myocardial stiffness in health and disease.Nature cardiovascular research · 2022Review
- Transient activation of PKC results in long-lasting detrimental effects on systolic [CaJournal of molecular and cellular cardiology · 2018Article
- MicroRNA-140 is elevated and mitofusin-1 is downregulated in the right ventricle of the Sugen5416/hypoxia/normoxia model of pulmonary arterial hypertension.American journal of physiology. Heart and circulatory physiology · 2016Article
- Detyrosinated microtubules buckle and bear load in contracting cardiomyocytes.Science (New York, N.Y.) · 2016Article
- Microtubule proliferation in right ventricular myocytes of rats with monocrotaline-induced pulmonary hypertension.Journal of molecular and cellular cardiology · 2013Article
- Mechanical modulation of cardiac microtubules.Pflugers Archiv : European journal of physiology · 2011Review
- Proliferating cardiac microtubules.American journal of physiology. Heart and circulatory physiology · 2009Article
- Adenosine regulation of microtubule dynamics in cardiac hypertrophy.American journal of physiology. Heart and circulatory physiology · 2009Article
- Axial stretch of rat single ventricular cardiomyocytes causes an acute and transient increase in Ca2+ spark rate.Circulation research · 2009Article
- Cardiac dysfunction in aging conscious rats: altered cardiac cytoskeletal proteins as a potential mechanism.American journal of physiology. Heart and circulatory physiology · 2008Article
- Molecular basis of diastolic dysfunction.Heart failure clinics · 2008Review
- Stable microtubules contribute to cardiac dysfunction in the streptozotocin-induced model of type 1 diabetes in the rat.Molecular and cellular biochemistry · 2007Article
- The cytoskeleton and related proteins in the human failing heart.Heart failure reviews · 2000Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The Frank-Starling mechanism, by which load directly regulates muscle length and thus performance is the means by which the mechanics and energetics of cardiac muscle are regulated on a beat-to-beat basis. When this short-term compensation for increased load is insufficient, the long-term compensation of cardiac hypertrophy ensues. The simplest and most direct mechanism for load regulation of cardiac mass would obtain if an analog of the short-term Frank-Starling mechanism of functional regulation operated in the long-term time domain of mass regulation; that is, if heart muscle were able to directly transduce increased load into growth. It is now clear that load does indeed serve as a direct regulator of cardiac mass in the adult. Cardiac hypertrophy, at the levels of intact animal, isolated tissue, and cultured cells, is a direct response of the adult mammalian cardiocyte to increased load, modified by but without the requisite involvement of factors external to the cell. The extent to which such hypertrophy is compensatory is critically dependent on the type of hemodynamic overload that serves as the hypertrophic stimulus. Thus, cardiac hypertrophy is not intrinsically maladaptive; rather, it is the nature of the inducing load rather than hypertrophy itself that is responsible for the frequent deterioration of initially compensatory hypertrophy into the congestive heart failure state. As one example reviewed here of this load specificity of maladaptation, increased microtubule network density is a persistent feature of severely pressure overloaded, hypertrophied and failing myocardium which imposes a viscous load on active myofilaments during contraction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.