ArticleMolecular and cellular biochemistry2025
Nitric oxide induces apoptosis of human primary melanocytes by regulating calcium homeostasis via VDAC1.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Synthesis, Biological Evaluation, and Computational Study of Pyridine- and Indazole-Based Inhibitors of the Inducible Nitric Oxide Synthase as Promising Antipsoriatic Agents.ACS pharmacology & translational science · 2026Article
- Controlled Delivery of Gasotransmitters for Cardiovascular Therapy: Molecular Mechanisms, Engineered Platforms, and Translational Perspectives.International journal of nanomedicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Vitiligo is an autoimmune skin disease that originates from damage and loss of melanocytes (MCs). Studies have identified abnormal nitric oxide (NO) metabolism in vitiligo patients, but the mechanisms by which NO contributes to MC loss remain unclear. Skin samples from patients with vitiligo and healthy controls were collected to evaluate the expression of three nitric oxide synthases (NOS) isoforms. Keratinocytes, MCs, and fibroblasts were exposed to a cytokine cocktail (IFN-γ, TNF-α, IL-1β and LPS) to simulate the pro-inflammatory microenvironment of vitiligo. Then NOS activation and the capacity for NO production were examined in each cell type. Sodium nitroprusside (SNP) was used as the NO donor to evaluate its cytotoxic effects on MCs. Cell viability, trypan blue staining rate, and lactate dehydrogenase release were measured following SNP exposure. Ultrastructural changes in MCs were observed using transmission electron microscopy. Apoptosis rate, intracellular calcium concentration, and mitochondrial membrane potential were assessed using flow cytometry. BAPTA-AM was used for intracellular calcium chelation and small interfering RNA was used to silence VDAC1 expression in MCs. Inducible NOS (iNOS) expression was significantly upregulated in patients in the active vitiligo lesions. Under pro-inflammatory conditions, keratinocytes and fibroblasts produced increased NO via iNOS activation. MCs exposed to a high-NO environment displayed dose-dependent cellular damage. SNP-treated MCs showed ultrastructural features of apoptosis, including condensed nuclear chromatin and swollen mitochondria. Flow cytometry and analysis of pro-apoptotic markers confirmed mitochondrial-mediated apoptosis in MCs. Both calcium chelation and VDAC1 silencing alleviated the apoptosis of MCs by restoring calcium homeostasis and mitochondrial membrane potential. NO-induced apoptosis in MCs was mediated by calcium overload and mitochondrial dysfunction. iNOS activation may represent a contributor to melanocyte loss in vitiligo and a potential therapeutic target.
Indexed as
Identifiers
40753527What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.