Ask about this productRelated genes to: TNNI3 antibody
- Gene:
- TNNI3 NIH gene
- Name:
- troponin I3, cardiac type
- Previous symbol:
- CMD2A
- Synonyms:
- TNNC1, CMH7
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 1989-12-11
- Date modifiied:
- 2019-04-23
Related products to: TNNI3 antibody
Related articles to: TNNI3 antibody
- The cardiac sarcomere forms the fundamental contractile unit of the myocardium, and its precise structural and regulatory integrity is essential for normal cardiac function. Over the past several decades, advances in functional and structural biology, as well as molecular genetics, have improved our understanding of how sarcomeric protein dysfunction gives rise to inherited cardiomyopathies. This review combines current knowledge on sarcomere-associated hypertrophic cardiomyopathy and dilated cardiomyopathy, focusing on clinical presentation, genetic basis, and the mechanisms that link pathogenic variants to phenotypic manifestations. We highlight how disease-associated variants in sarcomeric genes, such as MYBPC3, MYH7, TNNC1, TNNI3 and TNNT2, perturb force generation, calcium handling, and myofilament turnover, ultimately driving hypertrophic or dilated phenotypes through distinct, yet overlapping, molecular cascades. Emerging sarcomere-targeted small molecular and gene therapies are discussed, including small-molecule myosin modulators, RNA-based strategies, and in vivo gene-editing approaches aimed at halting or reversing disease progression. These sarcomere-directed precision therapeutics are promising avenues in the treatment of inherited cardiomyopathies and other cardiovascular diseases. - Source: PubMed
Publication date: 2026/07/07
Shi YunBalint Brittany NNieto Morales Paula FLandstrom Andrew P - Severe cardiomyopathies in children may often demand a treatment with inclusion of mechanical circulatory support (MCS) or heart transplantation (HTx). Although these cardiomyopathies are not always hereditary, myocarditis may be regarded as a likely cause, if clinical course is not chronic. The aims of the study were to determine the genetic profile and prevalence of myocarditis in a pediatric population with clinical signs of severe cardiomyopathy. - Source: PubMed
Publication date: 2026/07/03
Milting HendrikGärtner AnnaWiebe CarolineManuylova TatianaKlingel KarinHabich LouisaHitz MarcTiesmeier JensLaser Lea ValescaZu Knyphausen EdzardYusenko MariaNguyen Hoa Huu PhucFoth RudiSandica EugenSchubert StephanLaser Thorsten - - Source: PubMed
Cutore LuigiValadà GiuseppeLeonardi GiuseppeZappulla PaoloCapodanno Davide - Pathological cardiac hypertrophy is a major precursor to heart failure, yet the transcriptional mechanisms that restrain maladaptive remodeling remain incompletely defined. Class IIa histone deacetylases (HDAC4, HDAC5, and HDAC9) modulate cardiac hypertrophy but exhibit paradoxical effects, underscoring the need for more precise therapeutic targets. Unlike other Class IIa HDACs, HDAC7 is not expressed in adult cardiomyocytes (CMs), and its role in cardiac stress responses is unknown. - Source: PubMed
Publication date: 2026/06/05
Bu JinHand Sophie MGuo ShuliangJang JihyunLi Deqiang - Dilated cardiomyopathy (DCM) and arrhythmogenic cardiomyopathy (ACM) are progressive cardiac muscle disorders with phenotypic and genetic overlap. Although a male predominance is noted in DCM/ACM, it remains unclear whether this extends to specific genetic subtypes or reflects variation in disease stage and whether sex influences age-dependent disease onset across pediatric and adult groups. - Source: PubMed
Publication date: 2026/05/20
Stroeks Sophie L V MBart Nicole KRossano JosephClaggett BrianBeelen Nina JBuchan Rachel JDay SharleneFornaro AlessandraHalliday Brian PWheeler Matthew THammersley Daniel JHelms AdamHeymans Astrid B MHo Carolyn YKhan Sadiya SLin KimLota AmritMerlo MarcoMestroni LuisaOlivotto IacopoOwens AnjaliSeidman Christine EShore SupriyaSinnette CorineSinagra GianfrancoStevenson Lynne WStewart Garrick CTheotakis PantazisVenner Max F G H MWare James STaylor Matthew R GVerdonschot Job A JWilsbacher LisaPrasad SanjayHeymans Stephane RParikh Victoria NTayal UpasanaLakdawala Neal K