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Michael Raddatz @michaelraddatz.bsky.social · 07/06/2026

Looks like they started enrolling in ~2023 which probably plays a role—at that point the data was almost entirely in patients with DM as mentioned in other replies. I agree with you though if they started enrolling today.

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Journal of Clinical Investigation @jci.org · 08/01/2026

Clonal hematopoiesis of indeterminate potential (CHIP) is common in older individuals, but its connection with aortic valve stenosis was unclear. Wesley T. Abplanalp & team now show CHIP activates procalcific pathways in macrophages and promotes AVS: www.jci.org/articles/vie...

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James Pirruccello 🎃🦇🧹 @jamespirruccello.com · 19/12/2025

We did a deep dive into aortic stenosis genetics, and took first steps to understand the genetics behind normal human variation in flow across the aortic valve.

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University of California @uofcalifornia.bsky.social · 09/08/2025

The federal government’s demand of $1 billion from @UCLA would devastate the nation’s best public university, cut off life-saving care, halt tech and economic growth and reduce educational access. Stand with UC to protect our vital mission: www.universityofcalifornia.edu/get-involved...

universityofcalifornia.edu

Stand Up for UC

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Jaweed Kaleem @jaweedkaleem.bsky.social · 08/08/2025

BREAKING: The Trump administration is seeking $1 billion+ from the University of California to restore UCLA's frozen federal funding. The payout would far exceed any made by universities so far. UC has not agreed to it, sources say. www.latimes.com/california/s...

latimes.com

Trump seeking $1 billion fine from UCLA over antisemitism allegations

The Trump administration has proposed the University of California pay more than a $1 billion to settle antisemitism charges and restore frozen grant funding at UCLA.

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Michael Raddatz @michaelraddatz.bsky.social · 28/05/2025

9/9 In summary, IL-6 may play a beneficial role in cardiovascular adaptation, and this may impact cardiovascular adaptation to exercise in patients taking an IL-6 inhibitor for RA. Read the full paper in this month’s issue of #JACCBTS! doi.org/10.1016/j.ja...

doi.org

Redirecting

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Michael Raddatz @michaelraddatz.bsky.social · 28/05/2025

8/ Given the reported beneficial effects of IL-6i in coronary disease (doi.org/10.1016/j.ja...) & ongoing related trials in cardiovascular patients (e.g., clinicaltrials.gov/study/NCT061...), this work reminds us that IL-6 biology is complex. There may be a right time, place, & amount for IL-6. 🤔

doi.org

The clinical significance of interleukin‐6 in heart failure: results from the BIOSTAT‐CHF study

Aims Inflammation is a central process in the pathophysiology of heart failure (HF), but trials targeting tumour necrosis factor (TNF)-α were largely unsuccessful. Interleukin (IL)-6 is an important...

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Michael Raddatz @michaelraddatz.bsky.social · 28/05/2025

7/ While the LV mass and stroke volume increases were only significant in the TNFi group, only the IL-6i group had a significant ⬆️ in relative VO2 peak. This is counterintuitive given the role of cardiac output in VO2, but may be explained by positive effects of IL-6i outside of cardiac remodeling.

Table showing an increase in LVM, LVSV, and LVEDV in the TNFi group, and n increase in VO2 in the IL-6i group.

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Michael Raddatz @michaelraddatz.bsky.social · 28/05/2025

6/ After 12 weeks of exercise, they underwent repeat testing. There was a physiologic ⬆️ in LV mass in the exercise group among those using a TNFi, but not among those using an IL-6i. This supports the authors’ hypothesis that IL-6 signaling is important for exercise adaptation in RA patients. 💭

Dot plot showing an increase in LV mass among exercise patients in those receiving a TNFi

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Michael Raddatz @michaelraddatz.bsky.social · 28/05/2025

5/ Prior to the exercise regimen, patients underwent cardiac MRI and metabolic testing. As seen here and further summarized in the full manuscript, patients had normal cardiac MRI metrics, low rates of cardiac comorbidities, and below average fitness as measured by VO2 peak. 😮‍💨

Table summarizing baseline cardiac metrics

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Michael Raddatz @michaelraddatz.bsky.social · 28/05/2025

4/ Patients were then randomized, with half of the patients undergoing supervised 45-minute exercise sessions on an ergometer bicycle three times a week in addition to their usual activity. 🚴📆

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Michael Raddatz @michaelraddatz.bsky.social · 28/05/2025

3/ They enrolled pts 18-69 yrs old with RA stably treated with a TNFi or IL-6i for >4 months. Their RA had to be well-controlled ✅ measured by DAS28-ESR score & minimal corticosteroid use. Importantly, pts receiving IL-6i had more often & more frequently tried other prior biologics for RA control.

Table describing baseline characteristics of patients in the trial

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Michael Raddatz @michaelraddatz.bsky.social · 28/05/2025

2/ Given previously described beneficial effects of IL-6 during exercise (onlinelibrary.wiley.com/doi/10.1111/...), the authors hypothesized that patients receiving TNF inhibitors would see more beneficial cardiovascular adaptation from guided exercise than those receiving IL-6 inhibitors. 🫀💪

onlinelibrary.wiley.com

Anti‐inflammatory effects of exercise: role in diabetes and cardiovascular disease

Background Persistent inflammation is involved in the pathogenesis of chronic diseases such as type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). Aims The aim of this review was to ...

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Michael Raddatz @michaelraddatz.bsky.social · 28/05/2025

In this month’s issue of #JACCBTS, Jønck, et al. explore the effects of cytokine inhibitors on cardiovascular adaptability in rheumatoid arthritis (RA). Read below to see what they found! 🧵 1/9 @jaccjournals.bsky.social

Title page of a paper titled IL-6 inhibitors and TNF inhibitors: Impact on Exercise-induced Cardiac Adaptations in Patients With Rheumatoid Arthritis

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Senator Chris Van Hollen @vanhollen.senate.gov · 18/04/2025

I said my main goal of this trip was to meet with Kilmar. Tonight I had that chance. I have called his wife, Jennifer, to pass along his message of love. I look forward to providing a full update upon my return.

Photo of Senator Chris Van Hollen with Kilmar Abrego Garcia.

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Boback Ziaeian @boback.bsky.social · 31/03/2025

The Lancet Commission on rethinking coronary artery disease: moving from ischaemia to atheroma Excited to have contributed to this work. #AHA25 www.thelancet.com/commissions/... @thelancet.bsky.social

thelancet.com

The Lancet Commission on rethinking coronary artery disease: moving from ischaemia to atheroma

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Michael Raddatz @michaelraddatz.bsky.social · 31/03/2025

Great manuscript and very informative figures!

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Michael Raddatz @michaelraddatz.bsky.social · 24/03/2025

10/10 In summary, diseased AVICs have mitochondrial dysfunction, and spermidine supplementation or DNMT1 inhibition might hold promise as therapeutics to reverse this process and treat valve calcification. Read the full paper in this month’s issue of #JACCBTS! www.sciencedirect.com/science/arti...

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Michael Raddatz @michaelraddatz.bsky.social · 24/03/2025

9/ The authors finally attempted to treat this same pathway through DNMT1 inhibition. They show that DNMT1 is ⬆️ with disease in human valves, as anticipated. Use of a DNMT1 inhibitor (5-Azacytidine) in diseased human AVICs increases SIRT1, PPARG, and markers of mitochondrial biogenesis. 📈

Human valve IHC showing increased DNMT1 expression in disease.

Box plots showing increase of DNMT1 and decrease of SIRT1, PPARG, and PGC1a in diseased AV cells. This is reversed with 5-AzaC.

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Michael Raddatz @michaelraddatz.bsky.social · 24/03/2025

8/ Returning to the initial mitochondrial phenotype, they show that spermidine improves mitochondrial function, even beyond healthy AVIC function. 🪃

Seahorse assay showing decreased respiration in diseased cells. Spermidine treatment augments respiration beyond both healthy and diseased cells. Bar charts showing a similar pattern with ATP production and coupling efficiency.

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Michael Raddatz @michaelraddatz.bsky.social · 24/03/2025

7/ Back in the dish, they showed that spermidine induces the same molecular changes in AVICs. 🧫

Box plots showing increased pAKT/AKT and DNMT1 in diseased cells and decreased TP53, SIRT1, and PPARG. These patterns are reversed with spermidine.

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Michael Raddatz @michaelraddatz.bsky.social · 24/03/2025

6/ They confirmed the expression patterns of TP53 ⬆️, SIRT1 ⬆️, DNMT1 ⬇️, and PPARG ⬆️ directly in the AVs from mice treated with spermidine or water.

Bar charts showing protein expression data of TP53 increased, SIRT1 increased, DNMT1 decreased, and PPARG increased with spermidine treatment.

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Michael Raddatz @michaelraddatz.bsky.social · 24/03/2025

5/ They next performed LC-MS proteomics on AVs from 🐭 with and without spermidine supplementation. They identified activation of the oxidative phosphorylation protein pathway. Further network analysis identified DNMT1 as a ⬇️ node, and PPARG, SIRT1 and TP53 as ⬆️ with spermidine.

Horizontal bar chart showing oxidative phosphorylation as the only positive Z-score protein set.

Network analysis showing DNMT1 and PPARG relationship and confidently predicted inhibition and activation respectively.

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Michael Raddatz @michaelraddatz.bsky.social · 24/03/2025

4/ They translated this in vitro finding to an Ldlr-/- and high-fat diet (HFD)-fed 🐭 model of CAVD and found improved echocardiographic metrics of aortic stenosis (AV peak gradient) and ⬇️ valve calcification and fibrosis with spermidine treatment.

Experimental model with an Ldlr-/- mouse treated with HFD and either water or spermidine. Box plots show increasing peak gradient with aging in the water-treated mice, that is not present in mice treated with spermidine.

Alizarin red staining of aortic valves and bar charts showing increase in AV thickness, MT stain, COL1, and Alizarin red in the Ldlr-/- & HFD disease model that is reversed with spermidine.

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Michael Raddatz @michaelraddatz.bsky.social · 24/03/2025

3/ The authors hypothesized that spermidine could be used to augment mitochondrial function (💪 read more: pubmed.ncbi.nlm.nih.gov/29371440/). They first showed that spermidine ⬇️ expression of calcification-related genes, both in diseased AVICs and in osteogenic media. 🧫

Box plots showing increase of ALP, Osteocalcin, RUNX2, and COL1A1 expression in diseased cells, which is reversed with treatment with spermidine. Alizarin red staining shows an increase with osteogenic media that is reversed with spermidine.

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Michael Raddatz @michaelraddatz.bsky.social · 24/03/2025

2/ The authors use a model system of aortic valve interstitial cells (AVICs) isolated from humans with and without calcific aortic valve disease (CAVD). They show that mitochondrial respiration, ATP production, coupling efficiency, and mitochondrial mass are all ⬇️ in diseased AVICs. 🪫

Seahorse assay showing decreased respiratory capacity in diseased AVICs. Bar charts showing decresaed ATP production, coupling efficiency, and mitochondrial staining with MitoTracker.

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Michael Raddatz @michaelraddatz.bsky.social · 24/03/2025

In these uncertain times, celebrating novel science is one way to stay grounded and hopeful. In this month’s issue of #JACCBTS, Song, et al. investigate mitochondrial function in aortic valve calcification. Join me to see what they found! 🧵 1/10 @jaccjournals.bsky.social

Title page of a paper titled Spermidine Enhances Mitochondrial Function and Mitigates Aortic Valve Calcification

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Altmetric @altmetric.com · 13/03/2025

Mike spotted this before the rest of us. 🫡 Publications from 2025 are shared more on Bluesky than on X/Twitter.

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Jeremy Berg @jeremymberg.bsky.social · 11/03/2025

I have confirmation from several sources now that all T32s, many F30s and F31s, and most or all Center awards (P30, P50) have been terminated at Columbia. This is quite damaging to research and to individuals. This is pure terrorism and cannot be legal. But litigation will take time...

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Justin Hendrix @justinhendrix.bsky.social · 09/03/2025

List includes Harvard University, George Washington University, Johns Hopkins University, New York University, Northwestern University, the University of California, Los Angeles; the University of California, Berkeley, the University of Minnesota, and the University of Southern California.

nytimes.com

Trump Pulled $400 million From Columbia. Other Schools Could Be Next.

The administration has circulated a list that includes nine other campuses, accusing them of failure to address antisemitism.

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Jack Iwashyna @iwashyna.bsky.social · 08/03/2025

NIH budget: $ 48b Musk wealth: $351b Both are mostly funded by your tax dollars But only one might save your life . . . . Sources: www.nih.gov/about-nih/wh... Search results: elon musk net worth g.co/kgs/6c8YEuB @standupforscience.bsky.social

g.co

Google Search

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Amy Klobuchar @amyklobuchar.com · 01/03/2025

During Rare Disease Week, patients and advocates were in D.C. for an event with the NIH, FDA, and HHS to highlight work being done on treatments and cures. It was abruptly canceled. Why? The administration fired the people organizing this important event and advancing this work.

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Duke University School of Medicine @dukemedschool.bsky.social · 21/02/2025

Duke is one of the largest biomedical research enterprises in the country. A cut of this magnitude (15%cap on F&As) would result in thousands of lost jobs at Duke & potentially tens of thousands across NC. Sources: medschool.duke.edu/about-us/fac... & www.unitedformedicalresearch.org/nih-pdf/?sta...

“This is seismic. Think of a car being built. The direct portion of any NIH grant goes toward the car components, but the indirect payments pay for the assembly line — the facilities, the specialty equipment, the IT structures, and the people. The F&A payments are essential; they are required to do the work.”

Colin S. Duckett, PhD, Executive Vice Dean for Basic and Preclinical Science, Duke University School of Medicine, on the devastating effects of the NIH’s cap on indirect grant payments.

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Eric Topol @erictopol.bsky.social · 24/01/2025

Welcome immigrants from X interested in science to the friendlier skies of @bsky.app, as documented by a new @nature.com survey (but you already knew that 😉) "Bluesky is much better for science. There is much less toxicity, misinformation, and distractions." www.nature.com/articles/d41...

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Michael Raddatz @michaelraddatz.bsky.social · 27/01/2025

9/9 In summary, CRP-rich plasma from Long COVID patients ⬆️ platelet activation, and platelet activation correlates with the severity of 🫁 damage. Platelet activation is reversible with aspirin or P2Y12. Read the paper in this month’s issue of #JACCBTS! doi.org/10.1016/j.ja...

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Michael Raddatz @michaelraddatz.bsky.social · 27/01/2025

8/ Aspirin or a P2Y12-inhibitor also reversed the platelet activation effects of Long COVID plasma, suggesting that these readily available treatments could be useful in this disorder.

Bar charts showing P-selectin positivity and PGA % increased with Long COVID plasma and this is reversed with aspirin or P2Y12 inhibitor treatment.

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Michael Raddatz @michaelraddatz.bsky.social · 27/01/2025

7/ The authors showed that platelet activation was further potentiated by IL-6 in the presence of CRP, thus they attempted to inhibit 🛑 platelet activation through CRP and IL-6. Platelet activation was reversed with FcgRi or tocilizumab, inhibiting CRP and IL-6, respectively.

Bar charts showing increased P-selectin positivity with CRP treatment that is augmented by increasing doses of IL-6, and inhibition of P-selectin positivity and PGA % with treatment with FCyRi or Tocilizumab among platelets treated with Long COVID plasma.

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Michael Raddatz @michaelraddatz.bsky.social · 27/01/2025

6/ They hypothesized that circulating factors were priming platelets in Long COVID patients and treated platelets from healthy subjects with different types of plasma. Indeed, Long COVID plasma ⬆️ P-selectin expression and PGAs in otherwise healthy platelets.

Bar charts showing P-selectin positivity and PGA are increased in Long COVID plasma-treated platelets compared to those treated with COVID Recovered plasma or autologous plasma.

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Michael Raddatz @michaelraddatz.bsky.social · 27/01/2025

5/ PGA and PMA also correlated with parenchymal lung damage in these patients. 🫁

Dot plots showing correlation of PMA and PGA with residual parenchyma damage

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Michael Raddatz @michaelraddatz.bsky.social · 27/01/2025

4/ Compared to both COVID recovered patients and healthy subjects, Long COVID patients had ⬆️ measures of platelet activation, including platelet-granulocyte aggregates (PGA) and platelet-monocyte aggregates (PMA).

Bar charts showing P-selectin positivity, PGA, and PMA are elevated in COVID Recovered and further elevated in Long COVID.

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Michael Raddatz @michaelraddatz.bsky.social · 27/01/2025

3/ Across patient groups, those with Long COVID and Acute COVID had ⬆️ CRP compared to recovered patients. Acutely infected patients also had ⬆️ IL-6, D-Dimer, and fibrinogen, which were not elevated in Long COVID.

Bar charts showing increased CRP, IL-6, D-dimer, and Fibrinogen in Acute COVID. CRP is also elevated in Long COVID.

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Michael Raddatz @michaelraddatz.bsky.social · 27/01/2025

2/ The authors previously showed in #JACCBTS that post-COVID pts have ⬆️ platelet activation: www.jacc.org/doi/10.1016/.... However, they looked to test this in Long COVID syndrome. Long COVID patients in this study were those who continued to have symptoms 6 mos post-infection. 🤒

jacc.org

Platelet and Endothelial Activation as Potential Mechanisms Behind the Thrombotic Complications of COVID-19 Patients:

Discover why JACC is the ultimate publishing partner for your cardiovascular research.

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Michael Raddatz @michaelraddatz.bsky.social · 27/01/2025

In this month’s issue of #JACCBTS, Brambilla, et al. explore the role of platelet function in long COVID. Read below ⬇️ to see what they found! 🧵 1/n @jeffhsumd.bsky.social @jaccjournals.bsky.social @vascularimmuno.bsky.social @jeanwassenaar.bsky.social

Title page of paper entitled "Low-Grade Inflammation in Long COVID Syndrome Sustains a Persistent Platelet Activation Associated With Lung Impairment"

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