Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The mitophagy receptor BNIP3L/Nix coordinates nuclear calcium signaling to modulate the muscle phenotype

10 Mar 2025

Abstract excerpt

Mitochondrial quality control is critical in muscle to ensure contractile and metabolic function. BNIP3L/Nix is a BCL2 member, a mitophagy receptor, and has been implicated in muscle atrophy. Human genome-wide association studies (GWAS) suggest altered BNIP3L expression could predispose to mitochondrial disease. To investigate BNIP3L function, we generated a muscle-specific knockout model. bnip3l knockout mice...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autophagy in Disease and Therapy
Share to Muscle Physiology and Disorders
Share to Sirtuins and Resveratrol in Medicine

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 40063005
DOI: 10.1080/15548627.2025.2476872

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The mitophagy receptor BNIP3L/Nix coordinates nuclear calcium signaling to modulate the muscle phenotypePMID 40063005Read ↗

The mitophagy receptor BNIP3L/Nix coordinates nuclear calcium signaling to modulate the muscle phenotypeSemantic proximity Read ↗

Bnip3 in mitophagy: Novel insights and potential therapeutic target for diseases of secondary mitochondrial dysfunctionSemantic proximity Read ↗

In Brief: Mitophagy: mechanisms and role in human diseaseSemantic proximity Read ↗

Coordination of mitochondrial and lysosomal homeostasis mitigates inflammation and muscle atrophy during agingSemantic proximity Read ↗

A mitochondrial SCF-FBXL4 ubiquitin E3 ligase complex restrains excessive mitophagy to prevent mitochondrial diseaseSemantic proximity Read ↗

DNM1L-mediated fission governs mitophagy & mitochondrial biogenesis during myogenic differentiationSemantic proximity Read ↗

Mitochondrial autophagy: Origins, significance, and role of BNIP3 and NIXSemantic proximity Read ↗

Mitochondrial Pruning by Nix and BNip3: An Essential Function for Cardiac-Expressed Death FactorsSemantic proximity Read ↗

FBXL4 mutations cause excessive mitophagy via BNIP3/BNIP3L accumulation leading to mitochondrial DNA depletion syndrome.Semantic proximity Read ↗

FBXL4 suppresses mitophagy by restricting the accumulation of NIX and BNIP3 mitophagy receptorsSemantic proximity Read ↗

Tumor suppressor functions of BNIP3 and mitophagySemantic proximity Read ↗

Role of BNIP3 and NIX in cell death, autophagy, and mitophagySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.