Scott Soleimanpour

🎉Early Career Researcher Grants for #MitoCellFate are now available💰
For more details on how to apply, please see the conference website here: bit.ly/43EWiSX
Be quick! Our short talk submission deadline is soon approaching (10 Nov 2025)
#FusionStemCells #FusionAgingResearch

Assessment of mitophagy in the Malphigian tubules of the dmt-Keima Drosophila kidney

In this week's issue of mitophagy news 🗑️🪫

biomed.news/bims-tofagi/...

-High sugar diet inhbits renal mitophagy and disrupts renal function
-a review by @soleimanpourlab.bsky.social on mitophagy in diabetic ß-cells
-Optineurin is necessary for mitochondrial removal during erythrocyte maturation

New from us! Had a question about mitophagy but were afraid to ask? 😂

Excited to review the latest advances in beta cell mitophagy research as a key adaptive response in all forms of diabetes in
@cp-trendsendomet.bsky.social. We'd be honored if you have it a read! #T1D #T2D

Mitophagy defects also negatively alter the ER redox environment. Not the most profound statement, but ER-mito crosstalk/cascades are likely a very important contributor to diabetes!

Thank you and excellent question! Misfolded proinsulin and ER stress definitely will elicit mito changes. Akita mice also have mito structural defects. In other cell types, ER stress causes mito fusion (maybe to compensate)? We have not examined mitophagy in these models ourselves though.

Fusion with blood vessel organoids supports pancreatic islet function Nature Reviews Endocrinology, Published online: 22 October 2025; doi:10.1038/s41574-025-01201-0Fusion with blood vessel organoids supports pancreatic islet function

New content online: Fusion with blood vessel organoids supports pancreatic islet function

New from us! Had a question about mitophagy but were afraid to ask? 😂

Excited to review the latest advances in beta cell mitophagy research as a key adaptive response in all forms of diabetes in
@cp-trendsendomet.bsky.social. We'd be honored if you have it a read! #T1D #T2D

US PhD admissions shrink as fears over Trump’s cuts take hold Some doctoral programmes are admitting no students at all amid uncertainty about federal science funding.

Some doctoral programmes in the US are admitting no students at all amid uncertainty about federal science funding

go.nature.com/4o63boK

True!!!

Collaborative. Creative. Impactful. Come join us in Ann Arbor! For more information and application link see jobs.sciencecareers.org/job/675674/f...

Mitophagy in the adaptation to pancreatic β cell stress in diabetes Mitophagy is a crucial quality control process that preserves metabolic efficiency by selectively targeting damaged mitochondria for removal. Given the high metabolic demand of pancreatic β cells’ insulin secretion, disruption of mitophagy contributes to the mitochondrial dysfunction and β cell failure that are a common feature of both type 1 and type 2 diabetes (T1D and T2D). We review the impact of mitophagy on β cell responses to (patho)physiologic stressors that underlie the development of T1D and T2D. We examine how β cells engage mitophagy in the adaptive response to metabolic, inflammatory, and oxidative damage. We also dissect the importance of ubiquitin- and receptor-mediated mitophagy, methodological advances to quantify mitophagy in β cells, and ongoing efforts to pharmacologically target mitophagy to preserve β cell health and improve glycemic control.

Online Now: Mitophagy in the adaptation to pancreatic β cell stress in diabetes #trends #endocrinology #metabolism

Gene therapy-mediated overexpression of wild-type MFN2 improves Charcot-Marie-Tooth disease type 2A Charcot-Marie-Tooth disease type 2A (CMT2A) is the most common axonal CMT and is associated with an early onset and severe motor-dominant phenotype. CMT2A is mainly caused by dominant mutations in the...

Gene therapy-mediated overexpression of wild-type MFN2 improves Charcot-Marie-Tooth disease type 2A www.biorxiv.org/content/10.1...

TRAF6 integrates innate immune signals to regulate glucose homeostasis via Parkin-dependent and Parkin-independent mitophagy TRAF6 bridges innate immune signaling to mitophagy to promote glucose control during metabolic stress.

🚨How do mitochondria sense and respond to metabolic stress from the environment in diabetes? 🤔

In new work out in #ScienceAdvances, we show that innate immune signaling promotes β cell compensation for metabolic stress by engaging mitophagy. 🚨1/n
www.science.org/doi/10.1126/...

📢Last weeks #immunometabolism discoveries @biomednews.bsky.social ⬇️⬇️⬇️

biomed.news/bims-imicid/...

Many highlights inside!

incl. TRAF6 integrates innate immune signals to regulate glucose homeostasis via Parkin-dependent and Parkin-independent mitophagy

In this image, the color changes show accruing mitochondrial damage, marking the importance of quality control and removing damaged mitochondria in maintaining the optimal pool for β cell insulin secretion.

Researchers show that innate immune signaling forms a protective response to equip β cells with the means to compensate for metabolic stress in type 2 diabetes.

Learn more in this week’s issue of #ScienceAdvances: https://scim.ag/4q2qDEO

Congratulations Sara and team on the exciting new work!

Thank you so much, Martin!!! We really appreciate it.

Wow - super cool work @frisophagy.bsky.social! Congrats indeed! 🤩

Ubiquitin-mediated mitophagy regulates the inheritance of mitochondrial DNA mutations Mitochondrial synthesis of adenosine triphosphate is essential for eukaryotic life but is dependent on the cooperation of two genomes: nuclear and mitochondrial DNA (mtDNA). mtDNA mutates ~15 times as...

Exciting study from @frisophagy.bsky.social in @chinnery in the Chinnery lab @mrc-mbu.bsky.social. Congratulations to all authors involved in the study! #mitochondria

Ubiquitin-mediated mitophagy regulates the inheritance of mitochondrial DNA mutations | Science
www.science.org/doi/10.1126/...

My last post stuck in my drafts...finally, we are so grateful to the outstanding reviewers and editor for making our work better. And special thanks to @ella-maru.bsky.social for the beautiful images for the cover!

Thank you Francis, these kind words mean so much! It's been a ride this year for sure, mostly after many quiet years while we finished these off. And a UBC influence in there too, a paper of Bruce's gave us great inspiration for this work!

Thank you so much, Elias! We really appreciate it!

This work led by Elena Levi-D'Ancona, a recent PhD graduate in our lab, was our first cover and only possible due to our amazing team and outstanding collaborators, including @nesvilab.bsky.social and Orian Shirihai, and funding from NIDDK, Breakthrough T1D, and the VA! Thank you! 🤗🙌 2/fin

TRAF6 integrates innate immune signals to regulate glucose homeostasis via Parkin-dependent and Parkin-independent mitophagy TRAF6 bridges innate immune signaling to mitophagy to promote glucose control during metabolic stress.

🚨How do mitochondria sense and respond to metabolic stress from the environment in diabetes? 🤔

In new work out in #ScienceAdvances, we show that innate immune signaling promotes β cell compensation for metabolic stress by engaging mitophagy. 🚨1/n
www.science.org/doi/10.1126/...

Excited to be speaking at the #MitoCellFate Fusion Meeting next year. It's an outstanding program, please consider attending!

Cake

Celebrating 600

Islets for research

Yesterday we celebrated our 600th human research islet isolation in support of diabetes research (and then last night isolated the islets in the pic). I’m very fortunate to work with such a dedicated team! See more at www.isletcore.ca

Novel insights into the molecular underpinnings of islet cell dysfunction in #T1D highlighting pathways that may be leveraged to preserve residual β-cell function and modulate α-cell activity @bcellorg.bsky.social www.jci.org/articles/vie...

Pancreatic cancer-related diabetes and type 2 diabetes differ in multiple aspects of glucose homeostasis - Diabetologia Aims/hypothesis Pancreatic ductal adenocarcinoma-related diabetes mellitus (PDAC-DM) is a paraneoplastic syndrome with a poorly understood pathophysiology. PDAC-DM is often clinically confused with type 2 diabetes, resulting in delayed cancer detection and poorly individualised hyperglycaemia treatment. We investigated whether these forms of diabetes can be distinguished at the metabolic level. Methods Adults with either cancer treatment-naive PDAC-DM (n=28) or type 2 diabetes (n=97), and with diabetes onset within 3 years, underwent mixed-meal tolerance tests to investigate glucose metabolism. Outcomes included insulin sensitivity (Matsuda index), insulin secretion (insulinogenic index), beta cell function (oral disposition index), insulin clearance, and postprandial glucagon, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) responses. Results Compared with type 2 diabetes, individuals with PDAC-DM showed ~2.5-fold greater insulin sensitivity, ~81% lower insulin secretion and ~40% lower beta cell function. Insulin clearance was higher in the PDAC-DM group than the type 2 diabetes group, with and without adjustment for insulin sensitivity. Glucagon and GLP-1 levels increased after a meal in both groups, but levels were higher in the PDAC-DM group. GIP levels were similar between groups. The metabolic differences between groups persisted after adjustment for age, sex and BMI. Conclusions/interpretation PDAC-DM and type 2 diabetes are metabolically distinct, with different defects responsible for hyperglycaemia. PDAC-DM is characterised predominantly by insulin deficiency and displays higher insulin sensitivity than type 2 diabetes. There are also differences in alpha cell regulation and insulin clearance compared with type 2 diabetes. These findings identify biological characteristics that may have implications for individualised treatment of PDAC-DM and guide diagnostic biomarker discovery for early PDAC diagnosis. Graphical Abstract

PDAC associated #diabetes vs #T2D greater insulin sensitivity, ~81% lower insulin secretion and ~40% lower beta cell function #pancreaticcancer link.springer.com/article/10.1...

I have gotten a bit behind at sharing the lab’s latest work - this paper is now published - check it out! www.cell.com/cell-reports... Long story short: insulin is the major determinant of female fat storage, with a relatively minor effect on males.

α cells use both PC1/3 and PC2 to process proglucagon peptides and control insulin secretion α cells can generate and secrete both glucagon and GLP-1 with distinct processing enzymes to control metabolism.

Studies of prohormone convertase knockouts in mouse islets reveal plasticity in proglucagon processing to support intra-islet α cell-to-β cell communication, normally dominated by glucagon secretion www.science.org/doi/10.1126/...