In the not too distant past, myofilament research attracted considerable attention after the discovery that mutations in myofilament genes cause cardiomyopathies. However, basic research has not been completely translated into therapies. This viewpoint discusses the need to develop innovative and integrative technologies and generate translatable models to uncover the complex biology of myofilament proteins to advance the field.

The sarcomere, composed of myofilaments, is the fundamental contractile unit of striated skeletal and cardiac muscle.¹ Myofilaments, occupying 70% of heart tissue, are composed of thick and thin filament proteins. Post-translational modifications of myofilament proteins regulate the rate and force of contraction.² Mutations in myofilament proteins cause contractile dysfunction leading to cardiomyopathies.³ Therefore, studying the structure and function of myofilament proteins is essential to understand basic muscle physiology. Since the late 1800s, scientists have studied myofilament biology, and interest in these proteins dramatically increased after the discovery of a point mutation in myosin that caused hypertrophic cardiomyopathy.³ From the late 1990s to the early 2000s, scientists, flush with research funding, made several significant discoveries. Unfortunately, continued reductions in funding and changing interests have conspired to reduce the number of active muscle researchers and the enthusiasm to work in the muscle biology field. Yet, the need for muscle research remains high. The arrangement and interaction of thick and thin filament proteins in the myofilament are not completely defined.⁴ Increasing prevalence of heart failure demands new solutions. In response, the combination of advanced technology, improved scientific rigor, and interdisciplinary collaboration, including a renewed link to clinicians, is needed to reinvigorate myofilament research.

The early pioneers of this field laid the fundamental groundwork for our understanding of myofilament properties by testing conditions that affect muscle behavior. These findings were almost always based on the development of new techniques to study …

在不太遥远的过去，发现肌丝基因突变引起心肌病后，肌丝研究引起了相当大的关注。但是，基础研究尚未完全转化为疗法。该观点讨论了开发创新和整合技术并生成可翻译模型以揭示肌丝蛋白的复杂生物学以推进该领域的必要性。

由肌丝组成的肌节是横纹骨骼肌和心肌的基本收缩单位。¹肌丝，占心脏组织的70％，由粗细的细丝蛋白组成。肌丝蛋白的翻译后修饰可调节收缩的速率和力。²肌丝蛋白突变导致收缩功能障碍，导致心肌病。³因此，研究肌丝蛋白的结构和功能对于了解基本的肌肉生理至关重要。自1800年代后期以来，科学家们一直在研究肌丝生物学，发现肌球蛋白的点突变导致肥厚型心肌病后，对这些蛋白的兴趣急剧增加。³从1990年代末到2000年代初，科学家在研究经费的支持下取得了几项重大发现。不幸的是，资金的不断减少和兴趣的不断变化已合谋减少了活跃的肌肉研究人员的数量以及在肌肉生物学领域工作的热情。然而，肌肉研究的需求仍然很高。肌丝中粗细丝蛋白的排列和相互作用尚未完全定义。⁴心力衰竭的流行率不断提高，需要新的解决方案。因此，需要结合先进技术，提高科学严谨性和跨学科合作（包括与临床医生的新链接）来振兴肌丝研究。

该领域的早期开拓者通过测试影响肌肉行为的条件，为我们了解肌丝特性奠定了基础。这些发现几乎总是基于新技术的研究……