Exploring Novel Mitochondrial-Related Targets and Post-Translational Modifications for Alleviating Radiation-Induced Heart Damage

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About this Research Topic

Submission deadlines

  1. Manuscript Summary Submission Deadline 28 February 2026 | Manuscript Submission Deadline 31 May 2026

  2. This Research Topic is currently accepting articles.

Background

Radiation-induced heart damage (RIHD) is a serious cardiovascular side effect caused by radiotherapy, such as cardiac hypertrophy, myocardial fibrosis and cardiac remodeling. Mitochondrial dysfunctions, such as enhanced mitophagy, mtROS accumulation or decoupling of mito-ER (endoplasmic reticulum) contributes to the initiation and progression of RIHD. Although one notable therapeutic strategy for anti-cardiovascular disease in clinical use is based on β-receptor antagonist and ACEI, the treatment has not been demonstrated to enhance or improve the survival status of patients with RIHD. Therefore, it is of critical importance to identify novel mitochondrial-related targets that are specifically linked to RIHD.

Dual specificity tyrosine-phosphorylation-regulated kinase 1B (DYRK1B) and Calcium-binding and coiled-coil domain-containing protein 2 (Calcoco2) activate the fusion of mitochondrial and autophagic vesicle for lysosomal degradation, which are mainly located membranes of mitochondrial. However, the regulatory mechanisms for DYRK1B and Calcoco2 are still unclear, implying the existence of potential molecular mechanisms that can precisely regulate mitochondrial dysfunction by mediating struture or functions of DYRK1B or Calcoco2, ultimately achieving relief of RIHD. Post-translational modification (PTM) is considered as a balancing mechanism for regulating start and end of multiple pathophysiological processes, including Ubiquitination, SUMOylation or lactylation.

This Research Topic aims to deliver valuable insights regarding the development of novel targets for mitochondrial dysfunctions and possible PTM, which will contribute to further exploration and development of drug targets for improving RIHD. It will focus on two aspects: identification of new targets of mitochondrial dysfunction and elucidation of the traditional Chinese medical herbs regulating PTM for improvement of RIHD. We welcome submissions of the following article types: Brief Research Report, Data Report, General Commentary, Hypothesis & Theory, Methods, Mini Review, Opinion, Original Research, Perspective, Review, Technology and Code, covering, but not limited to, the following subtopics:

1. Identification of innovative targeted drugs with potential protein targets for RIHD, focusing on the regulation of mitophagy in vivo

2. Exploration and identification of novel PTM to RIHD

3. Elucidation of the molecular mechanisms underpinning mitochondrial dysfunctions to RIHD

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This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

  • Brief Research Report
  • Case Report
  • Clinical Trial
  • Editorial
  • FAIR² Data
  • General Commentary
  • Hypothesis and Theory
  • Methods
  • Mini Review

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Keywords: RIHD; Mitochondrial Mitophagy; DYRK1B; Post-translational modification (PTM)

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