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Transient receptor potential vanilloid 2 (TRPV2) plays a significant role in the onset and progression of heart failure. In this review, the authors summarize the recent findings on TRPV2 in cardiomyocytes and immune cells involved in the development of heart failure and discuss the current progress of drug development that is aimed at treating heart failure through targeting TRPV2.
Transient receptor potential cation channel subfamily V (TRPV) can be overexpressed in breast cancer. TRPV channels play important roles in breast cancer cell proliferation, migration, and cell death as well as the tumor microenvironment and cancer-associated pain. This review provides an overview of TRPV channels in the context of breast cancer.
Transient receptor ion channels have emerged as critical channels/receptors in numerous physiological and pathological conditions. In this paper the authors discuss our current understanding of the role of macrophage transient receptor potential channel subfamily V member 4 (TRPV4) in various inflammatory conditions.
More than 40 different neurological diseases are caused by microsatellite repeat expansions. Repeat-associated non-AUG (RAN) proteins are translated from different types of nucleotide repeat expansions. The authors review the pathological and molecular aspects of RAN protein accumulation for each RAN translation disorder, the correlation between disease pathology, the available in vivo models and the common features shared by some of the newly discovered RAN proteins.
Increasing lines of evidence have shown beneficial effects of physical exercise against or delay neurodegeneration. However, the mechanisms of their beneficial effects are confusing because it involves the connection between the brain and muscles. This review summarizes these findings and discusses the differential and common effects of aerobic versus resistance exercises.
In this review, the amyloid cascade is summarized along with the results of major clinical trials that have sought to target the amyloid cascade for therapeutic intervention. The distinction between theory, largely unaltered, and proof of concept that might temper the theory, is highlighted.
This review discusses the templated spread of α-synuclein (α-syn) pathology in neurodegenerative disease from the perspective of proteopathic α-syn seeds. Recent discoveries concerning the structure and cell biology of pathological α-syn aggregates are highlighted.
Brain inclusions of the microtubule-associated protein tau are prominent pathological features in a spectrum of neurodegenerative diseases. MAPT gene mutations that encodes tau can directly cause neurodegeneration. Herein, the authors review what is known about MAPT mutations dysfunctions with a focus on the prion-like properties of tau protein.
Neurodegenerative diseases evolve in multi-factorial manners, yet coherent paradigms are emerging. Both Tau and TDP-43 proteinopathies are linked to multiple upstream influences, and both are connected with numerous deleterious downstream endpoints. Gene variants can be either disease-specific, or, exert influence on the misfolding pathology itself rather than the upstream cause.
Leveraging an extensive panel of α-synuclein antibodies that targets a wide range of epitopes, the authors provide evidence that multiple system atrophy α-synuclein inclusions display distinct misfolded strain-like characteristics divergent from Lewy body diseases. The findings also indicate that in multiple system atrophy α-synuclein prion-like strains are likely inherently mutable.
